Deleng sumberé Ati

{{Infobox Anatomy |
  Name         = Ati |
  Latin        = jecur, iecer
|
  GraySubject  = 250 |
  GrayPage     = 1188 |
  Image        = Leber Schaf.jpg |
  Caption      = Ati [[wedhus]]: (1) lobus tengen, (2) lobus kiwa, (3) lobus mawa buntut, (4) lobus kuadratus, (5) arteri ati lan vena portal, (6) klanjer getah bening ati, (7) kanthong empedu. |
  Image2      = Surface projections of the organs of the trunk.png |
  Caption2    = Proyeksi lumahing organ torso, nuduhaké ati ing tengah |
  Width        = 240 |
  Precursor    = [[foregut]] |
  System       = |sistem pancernan
  Artery       = [[Hepatic artery proper|arteri hepatika]] |
  Vein         = [[vena hepatika]], [[portal vena hepatika]] |
  Nerve        = [[celiac ganglia]], [[vagus]]<ref>{{GeorgiaPhysiology|6/6ch2/s6ch2_30}}</ref> |
  Lymph        = |
  MeshName     = Ati |
  MeshNumber   = A03.620 |
  DorlandsPre  = |
  DorlandsSuf  = |
}}
[[Gambar:Liver_superior.jpg|thumb|300px|Ati iku organ gedhé dhéwé ing badané manungsa.]]

'''Ati''' ({{lang-el|ἡπαρ, hēpar}}) wujud [[klanjer]] gedhé dhéwé ing njero [[awak]], manggon ana njero gronggongan [[weteng]] sisih tengen, peneré ing sangisoré [[diafragma]]. Ati iku sawijining [[organ (anatomi)|organ]] ing [[vèrtebrata]], kalebu [[manungsa]]. Organ iki duwé peran wigati ing [[métabolisme]] lan duwé sapérangan fungsi ing awak/badan kalebu panyimpenan [[glikogen]], sintesis [[protéin plasma]], lan netralaké obat. Ati uga mrodhuksi [[bile]], kang wigati kanggo pancernan.

Adhedhasar fungsiné, ati uga kalebu minangka piranti èkskrèsi. Iki amarga ati mbiyantu fungsi [[ginjel]] kanthi cara mecah sapérangan senyawa kang asifat [[racun]] lan ngasilaké [[amonia]], [[urea]], lan [[asem urat]] kanthi mupangataké [[nitrogen]] saka [[asem amino]]. Prosès pamecahan senyawa racun déning ati diarani prosès [[detoksifikasi]].

[[Lobus]] ati kawangun saka [[sèl parenkimal]] lan [[sèl non-parenkimal]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/11729749
| title        = Cooperation of liver cells in health and disease.
| accessdate   = 2010-07-30
| work         = Medical University of Gdansk, Department of Histology and Immunology; Kmieć Z.
}}</ref> Sèl parenkimal ing ati diarani [[hepatosit]], manggoni watara 80% [[volume]] ati lan nglakokaké manéka fungsi utama ati. 40% sèl ati ana ing lobus sinusoidal. Hepatosit wujud sèl endodermal kang kastimulasi déning [[jaringan]] mesenkimal kanthi terus-terusan wiwit [[embrio]] nganti ngrembaka dadi sèl parenkimal.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/765644
| title        = An experimental analysis of liver development
| accessdate   = 2010-10-11
| work         = Douarin NM
}}</ref> Sakwéné wektu mau, dumadi paningkatan [[transkripsi]] [[mRNA]] [[albumin]] minangka stimulan proliferasi lan diferensiasi sèl endodermal dadi hepatosit.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/1764997
| title        = Hepatocyte differentiation initiates during endodermal-mesenchymal interactions prior to liver formation
| accessdate   = 2010-10-11
| work         = Section of Biochemistry, Brown University; Cascio S, Zaret KS
}}</ref>

Lumen lobus kawangun saka [[sèl endotelial#Ati|SEC]] lan dipanggoni déning 3 jinis sèl liya, kaya ta [[sèl Kupffer]], [[sèl Ito]], [[limfosit]] intrahepatik kaya ta [[sèl pit]]. Sèl non-parenkimal manggoni watara 6,5% volume ati lan mrodhuksi manéka substansi kang ngendhalèkaké akèh fungsi hepatosit.

Filtrasi wujud salah siji fungsi lumen lobus sinusoidal kang misahaké lumahing hepatosit saka [[getih]], [[sèl endotelial#Ati|SEC]] duwé kapasitas [[endositosis]] kang gedhé banget kanthi manéka [[ligan]] kaya ta [[glikoprotein]], [[komplèks imun]], [[transferin]] lan [[seruloplasmin]]. SEC uga duwé fungsi minangka sèl presenter [[antigen]] kang nyedhiakaké [[kluster diferensiasi|èksprèsi]] [[komplèks histokompatibilitas utama|MHC I]] lan MHC II kanggo [[sèl T]]. [[Sèkrèsi]] kang dumadi ngambah manéka [[sitokina]], [[eikosanoid]] kaya ta [[prostanoid]] lan [[leukotriena]], [[endotelin|endotelin-1]], [[nitrogen monoksida]] lan sapérangan komponèn ECM.

[[Sèl Ito]] ana ing jaringan perisinusoidal, wujud sèl kanthi akèh [[vesikel]] [[lemak]] ing njero [[sitoplasma]] kang ngiket SEC kuwat banget nganti mènèhaké lapisan gandha ing lumen lobus sinusoidal. Nalika ati ana ing kaanan normal, sèl Ito nyimpen [[vitamin A]] guna ngendhalèkaké kalenturan matriks èkstraselular kang diwangun mawa SEC, kang uga wujud kalenturan saka lumen sinusoid.

[[Sèl Kupffer]] ana ing jaringan intrasinusoidal, wujud [[makrofaga]] kanthi kamampuan [[endositosis|endositik]] lan [[fagositosis|fagositik]] kang ngéramaké. Sèl Kupffer sadina-dina interaksi karo matérial kang asalé saka [[saluran pancernan]] kang ngandhut [[larutan]] bakterial, lan nyegah aktivasi èfèk toksin senyawa mau menyang njero ati. Paparan larutan bakterial kang dhuwur, mligi paparan [[lipopolisakarida|LPS]], gawé sèl Kupffer nglakokaké [[sèkrèsi]] manéka [[sitokina]] kang micu prosès [[paradhangan]] lan bisa ngakibataké tatu ing ati. Sèkrèsi antarané ngambah [[spesi oksigèn reaktif]], [[eikosanoid]], [[nitrogen monoksida]], [[karbon monoksida]], [[faktor nekrosis tumor-alfa|TNF-α]], [[interleukin-10|IL-10]], minangka rèspon [[sistem kakebalan turunan|kakebalan turunan]] sajeroning fasa [[infèksi]] primèr.

[[Sèl pit]] wujud [[limfosit]] kanthi [[granula]] gedhé, kaya [[sèl NK]] kang manggon ing ati. Sèl pit bisa ngindhuksi pepati sanalika ing [[sèl tumor]] tanpa gumantung ing [[kluster diferensiasi|èksprèsi]] [[antigen]] ing [[komplèks histokompatibilitas utama]]. Aktivitas sèl pit bisa ditingkataké kanthi stimulasi [[interferon|interferon-γ]].

Saliyané iku, ing ati isih ana [[sèl T|sèl T-γδ]], sèl T-αβ lan [[sèl NKT]].

Sebutan medhis kang ana gandhéngané karo ati lumrahé diwiwiti nganggo ''hepat-'' utawa ''hepatik'' saka tembung [[basa Yunani|Yunani]] kanggo ati, ya iku ''hepar''.

== Sèl punca ==
Saliyané hepatosit lan sèl non-parenkimal, ing ati isih ana jinis sèl liya ya iku sèl intra-hepatik kang asring diarani [[sèl oval]],<ref name="PM12490302">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/12490302
| title        = The role of hepatocytes and oval cells in liver regeneration and repopulation
| accessdate   = 2010-08-01
| work         = Department of Pathology, University of Washington; Fausto N, Campbell JS.
}}</ref> dan [[hepatosit duktular]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/7599440
| title        = Ductular hepatocytes
| accessdate   = 2010-08-01
| work         = Medical College of Virginia, Virginia Commonwealth University; Sirica AE.
}}</ref> Régénerasi ati sawisé [[hepatektomi]] parsial, lumrahé ora nglibataké [[sèl progenitor]] intra-hepatik lan [[sèl punca]] èkstra-hepatik (hemopoietik), lan gumantung mung marang proliferasi hepatosit. Nanging sajeroning kaanan nalika proliferasi hepatosit kacandhet utawa katundha, sèl oval kang ana ing aréa periportal bakal ngalami proliferasi lan diferènsiasi dadi hepatosit diwasa.<ref name="PM12490302" /><ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18187050
| title        = Stem cells, cell transplantation and liver repopulation
| accessdate   = 2010-08-01
| work         = Marion Bessin Liver Research Center, Division of Hepatology, Department of Medicine, Albert Einstein College of Medicine of Yeshiva University; Oertel M, Shafritz DA.
}}</ref> Sèl oval wujud wangun diferènsiasi saka sèl progenitor kang ana ing aréa portal lan periportal, utawa [[kanal Hering]],<ref>{{cite web
| url          = http://www.nature.com/ng/journal/v40/n4/abs/ng.107.html
| title        = Hepatic progenitor cells, stem cells, and AFP expression in models of liver injury
| accessdate   = 2010-08-01
| work         = Division of Radiooncology, Deutsches Krebsforschungszentrum; Kuhlmann WD, Peschke P.
}}</ref> lan mung tinemu nalika ati ngalami [[cidra]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/16965562
| title        = Hepatic stem cells: a review.
| accessdate   = 2010-08-01
| work         = Department of Anatomical Pathology, University of Cape Town; Vessey CJ, de la Hall PM.
}}</ref> Proliferasi kang dumadi ing sèl oval bakal minangka saluran èkskrèsi kang ngubungaké aréa [[parenkima]] papan dumadiné karusakan ati karo [[saluran empedu]]. [[Epimorfin]], sawijining [[morfogen]] kang akèh tinemu duwé peran ing akèh organ epitelial, katoné uga duwé peran ing pambentukan saluran empedu déning sèl punca hepatik.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20305811
| title        = Epimorphin regulates bile duct formation via effects on mitosis orientation in rat liver epithelial stem-like cells
| accessdate   = 2010-10-11
| work         = Stem Cell and Regenerative Medicine Lab, Beijing Institute of Transfusion Medicine; Zhou J, Zhao L, Qin L, Wang J, Jia Y, Yao H, Sang C, Hu Q, Shi S, Nan X, Yue W, Zhuang F, Yang C, Wang Y, Pei X.
}}</ref> Sawisé iku sèl oval bakal kadiferensiasi dadi [[hepatosit duktular]]. Hepatosit duktular dianggep wujud sèl transisi kang magepokan antarané karo:<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/7599440
| title        = Ductular hepatocytes.
| accessdate   = 2010-08-01
| work         = Medical College of Virginia, Virginia Commonwealth University; Sirica AE.
}}</ref>
* [[metaplasia]] duktular saka [[hepatosit parenkimal]] dadi [[epitelium]] biliari intra-hepatik
* konvèrsi metaplasia saka epitelium duktular dadi hepatosit parenkimal
* diferensiasi saka [[sèl punca]] saka silsilah hepatosit
gumantung ing jinis gangguan kang nyerang ati.

Ing modhèl [[tikus]] kanthi 70% hepatektomi, lan indhuksi regenerasi hepatik kanthi [[asetilaminofluorena-2]], tinemu yèn [[sèl punca]] kang asalé saka [[sungsum balung mburi]] bisa kadiferensiasi dadi [[hepatosit]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/17383429
| title        = Bone marrow-derived hepatic oval cells differentiate into hepatocytes in 2-acetylaminofluorene/partial hepatectomy-induced liver regeneration.
| accessdate   = 2010-08-01
| work         = Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine,; Oh SH, Witek RP, Bae SH, Zheng D, Jung Y, Piscaglia AC, Petersen BE.
}}</ref><ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/10325227
| title        = Bone marrow as a potential source of hepatic oval cells.
| accessdate   = 2010-08-01
| work         = Department of Pathology, School of Medicine, University of Pittsburgh; Petersen BE, Bowen WC, Patrene KD, Mars WM, Sullivan AK, Murase N, Boggs SS, Greenberger JS, Goff JP.
}}</ref> kanthi médhiasi [[hormon]] [[faktor stimulasi koloni granulosit|G-CSF]] minangka [[kemokina]] lan [[mitogen]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/17681181
| title        = Granulocyte-colony stimulating factor promotes liver repair and induces oval cell migration and proliferation in rats.
| accessdate   = 2010-08-01
| work         = Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida; Piscaglia AC, Shupe TD, Oh SH, Gasbarrini A, Petersen BE.
}}</ref> Regenerasi juga dapat dipicu dengan D-[[galaktosamina]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/7504886
| title        = Activation, proliferation, and differentiation of progenitor cells into hepatocytes in the D-galactosamine modhèl of liver regeneration.
| accessdate   = 2010-08-01
| work         = Marion Bessin Liver Research Center, Albert Einstein College of Medicine; Dabeva MD, Shafritz DA.
}}</ref>

== Sèl imunologis ==
Ati uga duwé peran sajeroning [[sistem kakebalan]] kanthi akèhé sèl imunologis ing [[sistem retikuendotelial]] kang duwé fungsi minangka [[tapis]] [[antigen]] kang kagawa menyang ati liwat [[sistem portal ati]]. Papindhahan fasa [[infèksi]] saka fasa primèr dadi fasa akut, ditengeri déning ati kanthi ngedhunaké sekresi albumin lan ngunggahaké [[sekresi]] [[fibrinogen]]. Fasa akut kang terus-terusan bakal ngakibataké [[simtoma]] [[hipoalbuminemia]] lan [[hiperfibrinogenemia]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/8288951
| title        = The effect of prednisolone and a protéin-deficient diet on plasma albumin and fibrinogen in a turpentine-induced acute-phase reaction in rats
| accessdate   = 2010-08-02
| work         = Department of Internal Medicine, University of Berne; Ballmer PE, Studer H.
}}</ref>

Nalika ati cidra, [[sèl getih putih]] bakal distimulasi kanggo migrasi nuju ati lan bebarengan karo sèl Kupffer nyekresi [[sitokina]] kang gawé modhulasi prilaku sèl Ito.<ref>{{cite web
| url          = http://www.medscape.com/viewarticle/436461_3
| title        = Hepatic Stellate Cell in Fibrosis: Stellate Cell Activation
| accessdate   = 2010-10-16
| work         = Division of Liver Diseases, Mount Sinai School of Medicine; Scott L. Friedman
}}</ref> [[Sèl T pambantu|Sèl T<sub>H</sub>1]] mrodhuksi sitokina kang ngundhakaké rèspon kakebalan selular kaya ta [[interferon|IFN-gamma]], [[faktor nekrosis tumor|TNF]], lan IL-2. [[Sèl T pambantu|Sèl T<sub>H</sub>2]] suwaliké bakal mrodhuksi sitokina kang ngundhakaké rèspon kakebalan humoral kaya ta [[interleukin-4|IL-4]], [[interleukin-5|IL-5]], [[interleukin-6|IL-6]], [[interleukin-13|IL-13]] lan ngundhakaké rèspon [[fibrosis ati|fibrosis]]. Sitokina kang disekresi déning sèl T<sub>H</sub>1 bakal nyandhet diferensiasi [[sèl T]] dadi sèl T<sub>H</sub>2, suwaliké sitokina sekresi T<sub>H</sub>2 bakal nyandhet proliferasi sèl T<sub>H</sub>1. Mula rèspon kakebalan asring ditélakaké kapolarisasi menyang rèspon kakebalan selular utawa humoral, nanging durung tau kaloroné.

== Fungsi ati ==
Manéka jinis tugas kang dilakokaké déning ati, dilakokaké déning hepatosit. Nganti saiki durung tinemu organ liya utawa organ gawéan utawa piranti kang bisa nggantèkaké kabèh fungsi ati. Sapérangan fungsi ati bisa digantèkaké kanthi prosès [[dialisis ati]], nanging tèknologi iki isih terus dikembangaké kanggo perawatan panandhang [[gagal ati]].

Minangka [[klanjer]], ati ngasilaké:
* [[empedu]] kang nganti ½ liter saben dina. Empedu wujud cuwèran semu ijo lan rasané [[pait]], asalé saka [[hemoglobin]] [[sèl getih abang]] kang wis tuwa, kang banjur disimpen ing njero kanthong empedu utawa dièkskrèsi menyang [[duodenum]]. Empedu ngandhut [[kolesterol]], [[garam]] [[mineral]], garam empedu, pigmèn [[bilirubin]], lan [[biliverdin]]. [[Sekresi]] empedu migunani kanggo nyerna [[lemak]], ngaktifaké [[lipase]], mbiyantu daya absorpsi lemak ing usus, lan ngowahi dat kang ora larut sajeroning [[banyu]] dadi dat kang larut sajeroning banyu. Yèn saluran [[empedu]] ing ati kabumpet, empedu lumebu menyang parédharan getih saéngga kulit panandhang dadi semu kuning. Wong kang mangkono iku diarani nandhang lelara kuning.
* sapérangan gedhé [[asem amino]]
* [[faktor koagulasi]] [[fibrinogen|I]], [[protrombin|II]], [[proakselerin|V]], [[prokonvertin|VII]], [[protromboplastin beta|IX]], [[protrombinase|X]], [[faktor PTA|XI]]
* [[protéin C]], [[protéin S]] lan [[anti-trombin]]
* [[kalsidiol]]
* [[trigliserida]] liwat lintasan [[lipogenesis]]
* [[kolesterol]]
* ''insulin-like growth factor 1'' (IGF-1), sawijining [[protéin]] polipeptida kang duwé peran wigati sajeroning pertumbuhan awak ing sajeroning mangsa bocah lan tetep duwé èfèk anabolik ing wong diwasa.
* [[enzim]] [[arginase]] kang ngowahi [[arginina]] dadi [[ornitina]] lan [[urea]]. Ornitina kang dumadi bisa ngiket NH³ lan CO² kang asifat racun.
* [[trombopoietin]], sawijining [[hormon]] [[glikoprotein]] kang ngendhalèkaké prodhuksi [[keping getih]] déning [[sungsum balung mburi]].
* Ing triwulan awal pertumbuhan [[janin]], ati wujud organ utama sintesis [[sèl getih abang]], nganti tekan sakiwa-tengené sungsum balung mburi bisa njupuk alih tugas iki.
* [[albumin]], komponèn [[osmolar]] utama ing [[plasma getih]].
* [[angiotensinogen]], sawijining [[hormon]] kang duwé peran kanggo ngundhakaké [[tekanan getih]] nalika diaktivasi déning [[renin]], sawijining [[enzim]] kang disekresi déning [[ginjel]] nalika dikawruhi kurangé tekanan getih déning ''juxtaglomerular apparatus''.
* [[enzim]] [[aspartat transaminase|glutamat-oksaloasetat transferase]], [[alanina transaminase|glutamat-piruvat transferase]] lan [[laktat dehidrogenase]]

Saliyané nglakokaké prosès [[glikolisis]] lan [[siklus asem sitrat]] kaya sèl ing lumrahé, ati uga duwé peran sajeroning [[metabolisme karbohidrat]] liyané:
* [[Glukoneogenesis]], [[sintesis]] [[glukosa]] saka sapérangan [[substrat]] [[asem amino]], [[asem laktat]], [[asem lemak|asem lemak non ester]] lan [[gliserol]]. Ing [[manungsa]] lan sapérangan jinis [[mamalia]], prosès iki ora bisa ngonvèrsi gliserol dadi glukosa. Lintasan ditambah rikat déning [[hormon]] [[insulin]] sairing karo [[hormon]] [[tri-iodotironina]] liwat patambahan laju [[siklus Cori]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20519325
| title        = Insulin Action in Hyperthyroidism: A Focus on Muscle and Adipose Tissue.
| accessdate   = 2010-08-07
| work         = Hellenic National Center for Research, Prevention, and Treatment of Diabetes Mellitus and Its Complications, et al; Mitrou P, Raptis SA, Dimitriadis G.
}}</ref>
* [[Glikogenolisis]], lintasan [[katabolisme]] [[glikogen]] dadi [[glukosa]] kanggo dieculaké menyang getih minangka rèspon ningkaté kabutuhan ènèrgi déning awak. Hormon [[glukagon]] wujud stimulator utama keloro lintasan glikogenolisis lan glukoneogenesis nglirwakaké awak saka [[simtoma]] [[hipoglisemia]]. Ing modhèl tikus, defisiensi glukagon bakal nyandhet kaloro lintasan iki, nanging ngundhakaké [[toléransi glukosa]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20592160
| title        = Glucagon deficiency reduces hepatic glucose production and improves glucose tolerance in adult mice.
| accessdate   = 2010-08-07
| work         = Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia; Hancock AS, Du A, Liu J, Miller M, May CL.
}}</ref> Lintasan ini, bersama dengan lintasan glukoneogenesis padha [[saluran pencernaan]] dikendalikan olèh [[klanjer]] [[hipotalamus]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20561808
| title        = Hypothalamic integration of portal glucose signals and control of food intake and insulin sensitivity.
| accessdate   = 2010-08-07
| work         = Inserm U855, Institut national de la santé et de la recherche médicale, faculté de médecine Laennec; Delaere F, Magnan C, Mithieux G.
}}</ref>
* [[Glikogenesis]], lintasan [[anabolisme]] glikogen saka glukosa.

lan ing lintasan katabolisme:
* degradasi [[sèl getih abang]]. [[Hemoglobin]] kang kakandhut ing njeroné dipecah dadi [[wesi|dat wesi]], globin, lan [[heme]]. Dat wesi lan globin didhaur ulang, éwadéné heme dirombak dadi [[metabolit]] kanggo dièkskrèsi bebarengan [[empedu]] minangka [[bilirubin]] lan [[biliverdin]] kang warnané [[ijo]] semu biru. Ing njero [[usus]], dat empedu iki ngalami [[oksidasi]] dadi [[urobilin]] saéngga warna [[feses]] lan [[urin]] semu kuning.
* degradasi [[insulin]] lan sapérangan [[hormon]] liya.
* degradasi [[amonia]] dadi [[urea]]
* degradasi dat toksin kanthi lintasan [[detoksifikasi]], kaya [[metilasi]].

Ati uga nyadhangaké sapérangan substansi, saliyané glikogen:
* [[vitamin A]] (cadhangan 1–2 taun)
* [[vitamin D]] (cadhangan 1–4 sasi)
* [[vitamin B12]] (cadhangan 1-3 taun)
* [[wesi|dat wesi]]
* [[tembaga|dat tembaga]].

== Régénerasi sèl ati ==
Kamampuan ati kanggo nglakokaké régénerasi wujud sawijining prosès kang wigati banget supaya ati bisa pulih saka karusakan kang ditimbulaké saka prosès [[detoksifikasi]] lan imunologis. Régénerasi kagayuh kanthi interaksi kang komplèks banget antara [[sèl (biologi)|sèl]] kang ana sajeroning ati, ing antarané [[hepatosit]], [[sèl Kupffer]], [[sèl endotelial#Ati|sèl endotelial sinusoidal]], [[sèl Ito]] lan [[sèl punca]]; karo [[organ]] ekstra-hepatik, kaya ta [[klanjer tiroid]], [[klanjer adrenal]], [[pankreas]], [[duodenum]], [[hipotalamus]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20607568
| title        = Molecular mechanisms of liver regeneration and protection for treatment of liver dysfunction and diseases.
| accessdate   = 2010-07-30
| work         = Department of General Surgery, Hokkaido University School of Medicine; Fujiyoshi M, Ozaki M.
}}</ref>

Hépatosit, iku sèl kang unik banget. Potènsi hépatosit kanggo nglakokaké [[proliferasi]], muncul nalika dumadi kélangan [[massa]] sèl,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/12421677
| title        = The role of cytokines in liver failure and regeneration: potential new molecular therapies.
| accessdate   = 2010-07-30
| work         = The Goldyne Savad Institute for Gene Therapy, Hadassah Hebrew University Hospital,; Galun E, Axelrod JH.
}}</ref> kang diarani fasa prima utawa fasa kompetènsi réplikatif<ref name="PM8529831">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/8529831
| title        = Liver regeneration. 2. Role of growth factors and cytokines in hepatic regeneration
| accessdate   = 2010-07-30
| work         = Department of Pathology and Laboratory Medicine, Brown University,; Fausto N, Laird AD, Webber EM.
}}</ref> kang lumrahé dipicu déning sèl Kupffer liwat sekresi [[sitokina]] [[interleukin-6|IL-6]] lan [[faktor nekrosis tumor-alfa|TNF-α]]. Ing fasa iki, hepatosit ngleboni [[siklus sèl]] saka fasa G{{sub|0}} menyang fasa G{{sub|1}}.

TNF-α bisa mènèhaké èfèk proliferatif utawa apoptotik, gumantung ing [[spesi oksigèn réaktif]] lan [[glutathion]], minimal 4 [[faktor transkripsi]] diaktivasi sadurungé hepatosit lumebu menyang njero fasa proliferasi, ya iku [[NF-κB]], [[STAT-3]], [[AP-1]] lan [[C/EBP-beta]].<ref name="PM10728791">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/10728791
| title        = Liver regeneration.
| accessdate   = 2010-07-30
| work         = Department of Pathology, University of Washington School of Medicine; Fausto N.
}}</ref>

[[Proliferasi]] hépatosit diindhuksi déning stimulasi sitokina [[faktor pertumbuhan hépatosit|HGF]] lan [[hormon TGF|TGF-α]], lan [[hormon EGF|EGF]]<ref name="PM10728791" /> kanthi rong lintasan. HGF, TGF-α, lan EGF wujud faktor patuwuhan kang asalé saka [[substrat]] [[serina]] lan [[protéin]] [[logam]]<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/17013516
| title        = A molecular view of liver regeneration
| accessdate   = 2010-07-30
| work         = Department of Pathology, FMRP, USP, Brazil.; Tarlá MR, Ramalho FS, Ramalho LN, Silva Tde C, Brandão DF, Ferreira J, Silva Ode C, Zucoloto S.
}}</ref> kang ngindhuksi [[sintesis]] [[DNA]].<ref name="PM8529831" /> Lintasan pisanan ya iku lintasan IL-6/STAT-3 kang duwé peran sajeroning [[siklus sèl]] liwat [[siklin D1/p21]] lan pangreksan sèl kanthi paningkatan rasio [[Protein FLICE-i|FLIP]], Bcl-2, Bcl-xL, Ref1, lan MnSOD. Lintasan kaloro ya iku lintasan [[kinase fosfatidil inositol-3|PI3-K]]/[[PDK-1]]/[[kinase PB|Akt]] kang ngendhalèkaké ukuran sèl liwat [[molekul]] [[mTOR]], saliyané minangka dat anti-[[apoptosis]] lan [[antioksidan]].

[[Hormon]] [[tri-iodotironina]], saliyané ngedhunaké kadhar [[kolesterol]] ing ati,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20176747
| title        = Regulation of thyroid hormone activation via the liver X-receptor/retinoid X-receptor pathway
| accessdate   = 2010-08-01
| work         = Human and Natural Sciences Center, Federal University of ABC; Christoffolete MA, Doleschall M, Egri P, Liposits Z, Zavacki AM, Bianco AC, Gereben B.
}}</ref> uga duwé kapasitas sajeroning proliferasi hépatosit minangka mitogen kang duwé peran ing [[siklin D1]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18422700
| title        = Triiodothyronine stimulates hepatocyte proliferation in two models of impaired liver regeneration
| accessdate   = 2010-08-01
| work         = Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari,; Columbano A, Simbula M, Pibiri M, Perra A, Deidda M, Locker J, Pisanu A, Uccheddu A, Ledda-Columbano GM.
}}</ref> nambah rikat [[konsumsi]] [[oksigèn|O<sub>2</sub>]] déning [[mitokondria]] kanthi ngaktivasi [[transkripsi (genetik)|transkripsi]] ing [[gen]] [[ambegan]] nganti ngundhakaké prodhuksi [[spesi oksigèn réaktif]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20503439
| title        = Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress
| accessdate   = 2010-08-19
| work         = Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile; Videla LA.
}}</ref> [[Sekresi]] [[spesi oksigèn réaktif|ROS]] menyang njero [[sitoplasma]] hépatosit bakal ngaktivasi [[faktor transkripsi]] [[NF-κB]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/12885587
| title        = Thyroid hormone-induced oxidative stress triggers nuclear factor-kappaB activation and cytokine gene expression in rat liver.
| accessdate   = 2010-08-01
| work         = Programa de Farmacologíca Molecular y Clínica, Instituto de Ciencias Biomédicas, Universidad de Chile; Tapia G, Fernández V, Varela P, Cornejo P, Guerrero J, Videla LA.
}}</ref> Ing [[sèl Kupffer]], [[spesi oksigèn réaktif|ROS]] sajeroning sitoplasma, bakal ngaktivasi sekresi [[sitokina]] [[faktor nekrosis tumor-alfa|TNF-α]], [[interleukin-6|IL-6]] lan [[interleukin-1|IL-1]] kanggo disekresi. Ikatan kang dumadi antarané katelu sitokina iki karo hépatosit bakal ngindhuksi èksprèsi pancerep enzim [[antioksidan]], kaya ta [[mangan superoksida dismutase]], [[i-nitrogen monoksida sintase]], [[protéin anti-apoptosis]] Bcl-2, [[haptoglobin]] lan [[fibrinogen|fibrinogen-β]] kang diperlokaké hépatosit sajeroning proliferasi.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20503439
| title        = Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress.
| accessdate   = 2010-08-01
| work         = Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile; Videla LA.
}}</ref> [[Stres oksidatif]] kang bisa ditimbulaké déning ROS uga karusakan kang bisa ditimbulaké déning manéka sitokina, bisa diilangaké kanthi asupan [[tosoferol]] (100&nbsp;mg/kg) utawa senyawa panyandhet [[gadolinium klorida]] (10&nbsp;mg/kg) kaya kang diduwèni déning sèl Kupffer, sadurungé stimulasi hormon tri-iodotironina,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/16028366
| title        = Redox regulation of thyroid hormone-induced Kupffer cell-dependent IkappaB-alpha phosphorylation in relation to inducible nitric oxide synthase expression.
| accessdate   = 2010-08-01
| work         = Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile; Fernández V, Tapia G, Varela P, Videla LA.
}}</ref> éwadéné laju proliferasi hépatosit dikendhalèkaké déning kadhar [[etanolamina]] minangka [[faktor hepatotrofik humoral]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/9207089
| title        = Ethanolamine modulates the rate of rat hepatocyte proliferation in vitro and in vivo
| accessdate   = 2010-08-01
| work         = Meiji Institute of Health Sciences; Sasaki H, Kume H, Nemoto A, Narisawa S, Takahashi N.
}}</ref>

Kamampuan ati kanggo ngèlakokaké régenerasi wis dikawruhi wiwit jaman [[Yunani]] kuna saka carita [[mitos]] ngenani sawijining [[titan]] kang jenengé [[Prometheus (mitologi)|Prometheus]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1294986
| title        = The myth of Prometheus and the liver
| accessdate   = 2010-08-01
| work         = Department of Pathology, East Orange Veterans Affairs Medical Center; T S Chen dan P S Chen
}}</ref> Kamampuan iki bisa sirna, nganti hépatosit ora bisa lumebu menyang njero siklus sèl, sanajan kèlangan sapérangan massané, yèn dumadi [[fibrosis ati]]. Lintasan fibrosis kang ora énggal éntuk parawatan, saya suwé bakal ngrembaka dadi [[sirosis ati]]<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/19568569
| title        = Reversal of liver fibrosis
| accessdate   = 2010-08-01
| work         = Department of Internal Medicine, Division of Gastroenterology at King Fahad Hospital of the University; Ismail MH, Pinzani M.
}}</ref> lan ngudokaké panandhangé kanggo nglakoni [[transplantasi ati]] utawa [[hépatèktomi]] kanggo tetep urip.

Régenerasi ati sawisé hépatèktomi parsial wujud prosès kang rumit banget ing sangisoré prabawa owah-owahan [[hémodinamika]], [[modhulasi]] [[sitokina]], hormon faktor patuwuhan lan aktivasi [[faktor transkripsi]], kang ngarah ing prosès [[mitosis]]. Hormon [[laktogen|PRL]] kang di[[sekresi]] déning [[klanjer]] [[hipofisis]] ngindhuksi respon hépatotrofik minangka [[mitogen]] kang duwé peran sajeroning prosès [[proliferasi]] lan [[diferensiasi]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/19170064
| title        = Prolactin's role in the early stages of liver regeneration in rats.
| accessdate   = 2010-08-04
| work         = Departamento de Biología Molecular, Facultad de Ciencias C-V, Universidad Autónoma de Madrid; Olazabal IM, Muñoz JA, Rodríguez-Navas C, Alvarez L, Delgado-Baeza E, García-Ruiz JP.
}}</ref> PRL mènèhi prabawa marang paningkatan aktivitas [[faktor transkripsi]] kang duwé peran sajeroning proliferasi sèl, kaya ta [[AP-1]], [[c-Jun]] lan [[STAT-3]]; lan diferensiasi lan kareksané metabolisme, kaya ta [[C/EBP-alfa]], HNF-1, HNF-4 lan HNF-3. c-Jun wujud salah siji protéin panyusun [[AP-1]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/9792040
| title        = Signal transduction during liver regeneration
| accessdate   = 2010-08-04
| work         = Department of Medicine, University of North Carolina at Chapel Hill; Brenner DA.
}}</ref> Indhuksi [[NF-κB]] ing [[fasa]] iki diperlokaké kanggo nyegah [[apoptosis]] lan micu ''derap'' [[siklus sèl]] kang wajar.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/9466975
| title        = NFkappaB prevents apoptosis and liver dysfunction during liver regeneration
| accessdate   = 2010-08-04
| work         = Department of Medicine, The University of North Carolina at Chapel Hill,; Iimuro Y, Nishiura T, Hellerbrand C, Behrns KE, Schoonhoven R, Grisham JW, Brenner DA.
}}</ref> Ing wektu iki, peran [[retinil asetat]] dadi vital banget, amarga fungsiné kang nambah [[massa]] [[DNA]] lan protéin kang dikandhut.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1165330/pdf/biochemj00563-0218.pdf
| title        = Effect of Depletion of Vitamin A, followed by Supplementation with Retinyl Acetate or Retinoic Acid, on Regeneration of Rat Liver
| accessdate   = 2010-12-08
| work         = Department of Biochemistry, Indian Institute of Science; M. JAYARAM, K. SARADA dan J. GANGULY
| quote        = Although the rates of increase in the DNA and protéin contents reflected the rates of regeneration in all the groups, the RNA values followed a rather different pattern, in that they showed a striking increase immediately after supplementation with retinyl acetate (after the surgery),
}}</ref>

== Lelara ing ati ==
Ati wujud organ kang nopang kalangsungan urip mèh kabèh organ liya ing njero awak. Amarga papan kang strategis banget lan fungsi multi-dimensional, ati dadi rentan banget marang tekané manéka [[lelara]]. Ati bakal ngrèspon manéka lelara mau kanthi ngradhang, kang diarani [[hepatitis]]

Asring uga hepatitis diwiwiti karo réaksi [[radhang]] patobiokimiawi kang diarani [[fibrosis hati]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682233
| title        = Non-invasive assessment of liver fibrosis in chronic liver diseases: Implementation in clinical practice and decisional algorithms
| accessdate   = 2010-10-09
| work         = Department of Digestive Diseases, Hepatology and Clinical Nutrition, Dell’Angelo Hospital; Giada Sebastiani
| quote        = Formation and accumulation of fibrosis in the liver is the common pathway that leads to an evolutive liver disease
}}</ref> kanthi [[simtoma]] paraklinis wujud paningkatan rasio [[plasma getih|plasma]] [[laminin]], sawijining [[glikoprotein]] kang disekresi [[sèl Ito]], [[asem hialuronat]] lan sajenis [[aminopeptida]] ya iku [[kolagen|prokolagen]] jinis III,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/1651819
| title        = Biochemical markers of hepatic fibrosis.
| accessdate   = 2010-08-02
| work         = Department of Clinical Biochemistry, University of Padova; Plebani M, Burlina A.
}}</ref> dan [[antigen karsinoembrionik|CEA]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/1491181
| title        = Evaluation of the behavior of carcinoembryonic antigen in cirrhotic patients.
| accessdate   = 2010-08-02
| work         = Service of Internal Medicine, Hospital de Galdacano; Collazos J, Genollà J, Ruibal A.
}}</ref> Fibrosis ati bisa disebabaké déning asoré rasio plasma [[faktor patuwuhan hépatosit|HGF]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/17465748
| title        = Hepatocyte growth factor: a regenerative drug for acute hepatitis and liver cirrhosis
| accessdate   = 2010-07-28
| work         = Division of Molecular Regenerative Medicine, Department of Biochemistry and Molecular Biology, Osaka University Graduate School of Medicine; Mizuno S, Nakamura T.
}}</ref><ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15793283
| title        = Growth inhibition and apoptosis in liver myofibroblasts promoted by hepatocyte growth factor leads to resolution from liver cirrhosis
| accessdate   = 2010-07-28
| work         = Division of Molecular Regenerative Medicine, Course of Advanced Medicine, Osaka University Graduate School of Medicine; Kim WH, Matsumoto K, Bessho K, Nakamura T.
}}</ref> utawa amarga infèksi viral, kaya ta [[hepatitis B]], patogen kang disebabaké déning [[infèksi]] akut sajenis [[virus DNA]] kang duwé [[fokus infèksi]] wujud cithakan [[transkripsi]] kang diarani [[cccDNA]] kang ka[[metilasi]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/19475606
| title        = Evidence that methylation of hepatitis B virus covalently closed circular DNA in liver tissues of patients with chronic hepatitis B modulates HBV replication.
| accessdate   = 2010-08-02
| work         = State Key Laboratory of Cancer Biology, Department of Pharmacogenomics, School of Pharmacy, The Fourth Military Medical University; Guo Y, Li Y, Mu S, Zhang J, Yan Z.
}}</ref> utawa [[hepatitis C]], patogen sarupa hepatitis B kang disebabaké déning infèksi [[virus RNA]] kanthi fokus infèksi wujud [[metilasi DNA]], mligi liwat mékanisme [[èksprèsi gen]]etik [[gen|berkas]] [[GADD45B]], saéngga ngakibataké [[siklus sèl]] hépatosit dadi kacandhet-candhet.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20530689
| title        = Downregulation of Gadd45beta expression by hepatitis C virus leads to defective cell cycle arrest.
| accessdate   = 2010-08-02
| work         = Institut National de la Santé et de la Recherche Médicale U955; Higgs MR, Lerat H, Pawlotsky JM.
}}</ref><ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15509538
| title        = Hypermethylation of growth arrest DNA damage-inducible gene 45 beta promoter in human hepatocellular carcinoma.
| accessdate   = 2010-08-02
| work         = Department of Medical Oncology and Therapeutic Research, City of Hope National Medical Center; Qiu W, Zhou B, Zou H, Liu X, Chu PG, Lopez R, Shih J, Chung C, Yèn Y.
}}</ref>

Fibrosis ati merlokaké pananganan seawal mungkin, kaya ing modhèl [[tikus]], stimulasi proliferasi hépatosit bakal ngluruhaké fokus infèksi virus hepatitis B,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20578126
| title        = In vivo proliferation of hepadnavirus-infected hepatocytes induces loss of covalently closed circular DNA in mice.
| accessdate   = 2010-08-02
| work         = Department of Medicine, University Medical Center Hamburg-Eppendorf,; Lutgehetmann M, Volz T, Köpke A, Broja T, Tigges E, Lohse AW, Fuchs E, Murray JM, Petersen J, Dandri M.
}}</ref> sadurungé ngrembaka dadi [[sirosis ati]] utawa [[kanker ati|karsinoma hepatoselular]]. Sawisé dumadi kanker ati, [[senyawa organik|senyawa]] [[siklosporina]] kang duwé potènsi kanggo micu proliferasi hépatosit, malah bakal nyepetaké ngrembakané [[sèl kanker]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/8353842
| title        = Cyclosporine stimulates hepatocyte proliferation and accelerates development of hepatocellular carcinomas in rats
| accessdate   = 2010-08-01
| work         = Department of Pathology, University of Pittsburgh School of Medicine,; Masuhara M, Ogasawara H, Katyal SL, Nakamura T, Shinozuka H.
}}</ref> amarga sèl kanker ngalami [[hiperplasia]] hépatik, ya iku proliferasi kang ora dibarengi aktivasi [[faktor transkripsi]] genetik. Iki bisa diindhuksi mawa stimulasi [[timbal nitrat]] (LN, 100 mikromol/kg), [[siproteron asetat]] (CPA, 60&nbsp;mg/kg), lan [[nafenopin]] (NAF, 200&nbsp;mg/kg).<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/9049203
| title        = Liver cell proliferation induced by nafenopin and cyproterone acetate is not associated with increases in activation of transcription factors NF-kappaB and AP-1 or with expression of tumor necrosis factor alpha
| accessdate   = 2010-08-01
| work         = Dipartimento di Biochimica, Università di Verona; Menegazzi M, Carcereri-De Prati A, Suzuki H, Shinozuka H, Pibiri M, Piga R, Columbano A, Ledda-Columbano GM.
}}</ref>

Hépatitis uga bisa diwiwiti kanthi defisiensi [[mitokondria]] ing njero [[hepatosit]], kang diarani [[steatohepatitis]]. Disfungsi mitokondria bakal duwé dampak tumrap [[homeostasis]] senyawa [[lipid]] lan paningkatan rasio [[spesi oksigèn reaktif]] kang ngindhuksi [[faktor nekrosis tumor-alfa|TNF-α]].<ref name="PM15489566">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15489566
| title        = Mitochondrial injury in steatohepatitis.
| accessdate   = 2010-08-05
| work         = Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 481, Faculté de Médecine Xavier Bichat; Pessayre D, Fromenty B, Mansouri A.
}}</ref> Iki bakal terus ing pangendhepan [[lemak]], [[stres oksidatif]] lan [[peroksidasi lipid]],<ref name="PM18061659">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18061659
| title        = Mitochondrial involvement in non-alcoholic steatohepatitis.
| accessdate   = 2010-08-05
| work         = Department of Medical and Occupational Sciences, University of Foggia; Serviddio G, Sastre J, Bellanti F, Viña J, Vendemiale G, Altomare E.
}}</ref> sarta marakaké mitokondria dadi rentan marang pepati déning [[nekrosis]] akibat asoré rasio [[adenosina trifosfat|ATP]] sajeroning matrik mitokondria, utawa déning [[apoptosis]] liwat pambentukan [[apoptosom]] lan paningkatan [[permeabilitas]] membran mitokondria kanthi mekanisme Fas/[[faktor nekrosis tumor-alfa|TNF-α]]. Panyuwunan [[ènergi]] kang dhuwur ing kaanan iki njalari mitokondria ora bisa mulihaké cadhangan [[adenosina trifosfat|ATP]] nganti bisa micu [[sirosis ati]],<ref name="PM18061659" /> éwadéné peroksidasi lipid bakal njalari karusakan ing [[DNA]] mitokondria lan membran mitokondria sisih njero kang diarani [[sardiolipin]], kanthi paningkatan laju oksidasi-beta [[asem lemak]], bakal dumadi akumulasi [[èlèktron]] ing ''respiratory chain'' komplèks I lan III kang ngedhunaké kadhar [[antioksidan]].<ref name="PM15489566" />

Sèl hépatosit apoptotik bakal dicerna déning [[sèl Ito]] dadi [[fibrinogen]] kanthi réaksi [[fibrogenesis]] sawisé diaktivasi déning prodhuk saka peroksidasi lipid lan rasio [[leptin]] kang dhuwur. Apoptosis kronis banjur dikompènsasi kanthi paningkatan laju proliferasi hépatosit, dikanthèni [[DNA]] kang rusak déning disfungsi mitokondria, lan njalari [[mutasi]] genetik lan kanker.

Ing modhèl [[tikus]], [[melatonin]] wujud senyawa kang ngedhunaké [[fibrosis ati]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/19322917
| title        = Melatonin ameliorates experimental hepatic fibrosis induced by carbon tetrachloride in rats
| accessdate   = 2010-08-05
| work         = Department of Geriatrics Medicine, The First Affiliated Hospital of Anhui Medical University; Hong RT, Xu JM, Mèi Q.
}}</ref> sauntara ing modhèl [[klinci]], [[kurkumin]] wujud [[senyawa organik]] kang ngedhunaké paraklinis steatohepatitis,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/19539747
| title        = Curcumin ameliorates rabbits's steatohepatitis via respiratory chain, oxidative stress, and TNF-alpha.
| accessdate   = 2010-08-05
| work         = Department of Biochemistry and Molecular Biology II, 18071 University of Granada; Ramirez-Tortosa MC, Ramirez-Tortosa CL, Mesa MD, Granados S, Gil A, Quiles JL.
}}</ref> sauntara [[hormon]] [[serotonin]]<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/17681180
| title        = Serotonin mediates oxidative stress and mitochondrial toxicity in a murine modhèl of nonalcoholic steatohepatitis.
| accessdate   = 2010-08-05
| work         = Switserlan Hepato-Pancreato-Biliary Center, Department of Visceral and Transplantation Surgery, University Hospital Zurich; Nocito A, Dahm F, Jochum W, Jang JH, Georgiev P, Bader M, Renner EL, Clavien PA.
}}</ref> lan kurangé asupan [[metionina]] lan [[kolina]]<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15464239
| title        = Pentoxifylline attenuates steatohepatitis induced by the methionine choline deficient diet.
| accessdate   = 2010-08-05
| work         = Department of Medicine, Division of Hepatology, Feinberg School of Medicine, Northwestern University; Koppe SW, Sahai A, Malladi P, Whitington PF, Green RM.
}}</ref> mènèhi èfèk suwaliké kanthi [[resistansi adiponektin]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18534710
| title        = MCD-induced steatohepatitis is associated with hepatic adiponectin resistance and adipogenic transformation of hepatocytes.
| accessdate   = 2010-08-05
| work         = ANU Medical School, Ostralin National University at The Canberra Hospital,; Larter CZ, Yeh MM, Williams J, Bell-Anderson KS, Farrell GC.
}}</ref>

Disfungsi mitokondria uga tinemu ing kabèh [[patogenesis]] ati, saka kasus radhang nganti kanker lan transplantasi.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20491641
| title        = Targeting Mitochondria: A New Promising Approach for the Treatment of Liver Diseases
| accessdate   = 2010-08-05
| work         = Centre for the Study of Liver Diseases, Department of Medical and Occupational Sciences; Serviddio G, Bellanti F, Sastre J, Vendemiale G, Altomare E.
}}</ref> Ing [[kolestasis]] kronik, [[asem ursodeoksikolat]] bebarengan karo [[glutathion|GSH]] silih sinergis minangka [[antioksidan]] kang ngreksa [[sardiolipin]] lan [[fosfatidil serina]] nganti nyegah dumadiné sirosis ati.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/14999689
| title        = Ursodeoxycholic acid protects against secondary biliary cirrhosis in rats by preventing mitochondrial oxidative stress.
| accessdate   = 2010-08-05
| work         = Department of Medical and Occupational Sciences, University of Foggia; Serviddio G, Pereda J, Pallardó FV, Carretero J, Borras C, Cutrin J, Vendemiale G, Poli G, Viña J, Sastre J.
}}</ref>

=== Prabawa alkohol ===
Alkohol ditepungi duwé fungsi immunosupresif marang [[sistem kakebalan awak]], kalebu ngredhem èksprèsi [[kluster diferensiasi]] [[CD4]]<sup>+</sup> lan [[CD8]]<sup>+</sup> kang diperlokaké sajeroning njaga tahaning ati marang infèksi viral, mligi HCV.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893013
| title        = Hepatitis C Virus and Alcohol
| accessdate   = 2010-10-09
| work         = Warren Alpert Medical School of Brown University; Larry Siu, Julie Foont, dan Jack R. Wands
}}</ref> Alkohol uga ngredhem rasio [[kemokina]] [[interferon|IFN]] ing lintasan [[transduksi sinyal selular]], saliyané ngundhakaké résiko dumadiné fibrosis.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654191
| title        = Hazardous drinking is associated with elevated aspartate aminotransferase to platelet ratio index in an urban HIV clinical cohort
| accessdate   = 2010-10-09
| work         = Department of Medicine, Johns Hopkins University School of Medicine, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health; Amina A. Chaudhry, Mark S. Sulkowski, Geetanjali Chander, dan Richard D. Moore
}}</ref>

Akèh [[lintasan metabolisme]] mènèhi kontribusi marang alkohol kanggo ngindhuksi [[stres oksidatif]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2268632
| title        = CYP2E1 and Oxidative Liver Injury by Alcohol
| accessdate   = 2010-10-13
| work         = Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine; Yongke Lu dan Arthur I. Cederbaum
}}</ref> Salah siji lintasan métabolisme kang asring diaktivasi déning etanol ya iku indhuksi enzim [[sitokrom P450 2E1]]. Enzim iki nimbulaké [[spesi oksigèn réaktif]] kaya radikal anion superoksida lan [[hidrogen peroksida]], sarta ngaktivasi subtrat toksik kalebu etanol dadi prodhuk kang luwih réaktif lan toksik. [[Sèl dendritik]] katoné wujud sèl kang paling kaprabawa déning kandhutan [[etanol]] ing njero alkohol. Ing pacobèn migunakaké modhèl [[tikus]], etanol ngundhakaké rasio [[plasma getih|plasma]] [[interleukin-1|IL-1β]], [[interleukin-6|IL-6]], [[interleukin-8|IL-8]], [[faktor nekrosis tumor-alfa|TNF-α]], [[aspartat transaminase|AST]], [[alanina transaminase|ALT]], [[etanol dehidrogenase|ADH]], [[gamma glutamil transpeptidase|γ-GT]], [[trigliserida|TG]], [[malondialdehid|MDA]] lan ngredham rasio [[interleukin-10|IL-10]], [[glutathion|GSH]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900062
| title        = Protective effects of quercetin on liver injury induced by ethanol
| accessdate   = 2010-10-11
| work         = Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College; Xi Chen
}}</ref> [[faktor transkripsi]] [[NF-κB]] lan [[AP-1]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1765445
| title        = Ethanol prevents development of destructive arthritis
| accessdate   = 2010-10-11
| work         = Department of Rheumatology and Inflammation Research, Center for Bone Research at the Sahlgrenska Academy, Göteborg University, Section for Medical Inflammation Research, Lund University; Ing-Marie Jonsson, Margareta Verdrengh, Mikael Brisslert, Sofia Lindblad, Maria Bokarewa, Ulrika Islander, Hans Carlsten, Claes Ohlsson, Kutty Selva Nandakumar, Rikard Holmdahl, dan Andrej Tarkowski
}}</ref>

=== Prabawa alkaloid ===
[[Kopi]], salah siji komplèks [[senyawa organik|senyawa]] [[alkaloid]] saka golongan [[purina]] [[xantina]] karo [[asem klorogenat]] lan [[lignan]],<ref name="PM16399494">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/16399494
| title        = Coffee and type 2 diabetes: from beans to beta-cells
| accessdate   = 2010-10-12
| work         = Department of Nutrition, Harvard School of Public Health; van Dam RM
}}</ref> ing studi epidemiologis, disimpulaké minangka salah siji faktor pamudhun risiko dumadiné [[diabetes mellitus]] jinis 2,<ref name="PM17023692">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/17023692
| title        = Coffee, diabetes, and weight control
| accessdate   = 2010-10-12
| work         = Department of Health and Nutrition Sciences, Brooklyn College, City University of New York; Greenberg JA, Boozer CN, Geliebter A.
}}</ref><ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/14706966
| title        = Coffee consumption and risk for type 2 diabetes mellitus
| accessdate   = 2010-10-12
| work         = Harvard School of Public Health, Channing Laboratory, Harvard Medical School, and Brigham and Women's Hospital; Salazar-Martinez E, Willett WC, Ascherio A, Manson JE, Leitzmann MF, Stampfer MJ, Hu FB.
}}</ref> [[lelara Parkinson]], [[sirosis ati]] lan [[karsinoma hepatoselular]],<ref name="PM16507475">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/16507475
| title        = Coffee and health: a review of recent human research
| accessdate   = 2010-10-12
| work         = Linus Pauling Institute, Oregon State University; Higdon JV, Frei B
}}</ref> lan saya apiké [[toleransi glukosa]].<ref name="PM16399494" /> Konsumsi kopi kanthi kronis kabukti ora njalari [[tekanan getih dhuwur]] nanging kanthi akut ngakibataké paningkatan [[tekanan getih]] sauntara sajeroning selang wektu cendhak,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/2682780
| title        = Coffee and coronary heart disease: a review.
| accessdate   = 2010-10-12
| work         = Department of Medicine, University of Tennessee; Rosmarin PC
}}</ref> lan [[plasma getih|plasma]] [[homosisteina]]<ref name="PM16507475" /> saéngga bisa dadi ancaman kanggo panandhang gangguan kardiovaskular.<ref name="PM17023692" />

Konsumsi kopi kanthi teratur bisa ngedhunaké rasio enzim [[alanina transaminase|ALT]] sarta aktivitas enzimatik ing lintasan métabolisme ati,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/16491669
| title        = Coffee: good, bad, or just fun? A critical review of coffee's effects on liver enzymes
| accessdate   = 2010-10-13
| work         = Division of Gastroenterology, Hepatology, and Nutrition, Loyola University Medical Center; Homan DJ, Mobarhan S
}}</ref> kang asring disebabaké déning<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/8191101
| title        = [Increase of aminotransferases]
| accessdate   = 2010-10-13
| work         = Clinique médicale, CHU de Rouen; Trivalle C, Chassagne P, Doucet J, Perol MB, Landrin I, Manchon ND, Bourreille J, Bercoff E.
}}</ref> infèksi viral, indhuksi usada, [[karacunan]], kaanan iskemik, [[steatosis]] (akibat alkohol, diabetes, obesitas), lelara otoimun,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/12534025
| title        = [Interpretation of hypertransaminasemia]
| accessdate   = 2010-10-13
| work         = Service de médecine interne Hôpital Principal d'Instruction de Tunis; Othmani S, Bahri M, Bahri M.
}}</ref> lan [[sindrom resistansi insulin|resistansi insulin]], sindrom metabolisme,<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15810122
| title        = Contribution of metabolic factors to alanine aminotransferase activity in persons with other causes of liver disease
| accessdate   = 2010-10-13
| work         = Gastroenterology, Metabolism, Endocrinology and Nutrition, Department of Medicine, Veterans Affairs Puget Sound Health Care System; Ioannou GN, Weiss NS, Boyko EJ, Kahn SE, Lee SP.
}}</ref> lan kakèhen dat wesi.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15633120
| title        = Coffee and caffeine consumption reduce the risk of elevated serum alanine aminotransferase activity in the United States
| accessdate   = 2010-10-13
| work         = Social & Scientific Systems Inc.,; Ruhl CE, Everhart JE.
}}</ref> Saliyané ALT, kopi uga ngedhunaké enzim ati liyané, ya iku [[gamma glutamil transpeptidase|gamma-GT]] lan [[alkalina fosfatase]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/8104822
| title        = Unexpected effects of coffee consumption on liver enzymes.
| accessdate   = 2010-10-13
| work         = Istituto di Medicina Clinica, Università di Padova; Casiglia E, Spolaore P, Ginocchio G, Ambrosio GB.
}}</ref> lan mènèhi èfèk antioksidan lan detoksifikasi fasa II amarga senyawa [[diterpena]], [[kafestol]] lan [[kahweol]],<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18028974
| title        = Induction of cancer chemopreventive enzymes by coffee is mediated by transcription factor Nrf2. Evidence that the coffee-specific diterpenes cafestol and kahweol confer protection against acrolein.
| accessdate   = 2010-10-13
| work         = Biomedical Research Centre, Ninewells Hospital and Medical School, University of Dundee; Higgins LG, Cavin C, Itoh K, Yamamoto M, Hayes JD.
}}</ref> saéngga nyegah dumadiné prosès [[karsinogenesis]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18701223
| title        = The multifaceted mechanisms for coffee's anti-tumorigenic effect on liver.
| accessdate   = 2010-10-13
| work         = Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University; Tao KS, Wang W, Wang L, Cao DY, Li YQ, Wu SX, Dou KF.
}}</ref><ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/15713964
| title        = Influence of coffee drinking on subsequent risk of hepatocellular carcinoma: a prospective study in Japan
| accessdate   = 2010-10-13
| work         = Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center; Inoue M, Yoshimi I, Sobue T, Tsugane S; JPHC Study Group.
}}</ref> Prosès tersebut dibarengi dengan gamma-GT sebagai indikator utama.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18537182
| title        = Joint effects of coffee consumption and serum gamma-glutamyltransferase on the risk of liver cancer
| accessdate   = 2010-10-13
| work         = Department of Public Health, University of Helsinki; Hu G, Tuomilehto J, Pukkala E, Hakulinen T, Antikainen R, Vartiainen E, Jousilahti P.
}}</ref>

== Transplantasi ati ==
Tèknologi transplantasi ati wujud asil kang dikembangaké saka panlitèn ing sapérangan babagan studi kadhokteran. Ing taun 1953, [[Billingham]], [[Brent]], lan [[Medawar]] nemu yèn toléransi kimerisme<ref name="PM10833242">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/10833242
| title        = History of clinical transplantation.
| accessdate   = 2010-08-04
| work         = Thomas E. Starzl Transplantation Institute, University of Pittsburgh Medical Center,; Starzl TE.
}}</ref> bisa diindhuksi déning [[infus]] [[sèl hematolimfopoietik]] donor ing modhèl [[tikus]].<ref name="PM11200418">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/11200418
| title        = The mystique of hepatic tolerogenicity.
| accessdate   = 2010-08-04
| work         = Transplantation Institute, Departments of Surgery, Pathology, and Pediatrics, University of Pittsburgh Medical Center; Starzl TE, Murase N, Demetris A, Trucco M, Fung J.
}}</ref>

Nalika taun 1958 studi ''canine'' ngembangaké sawijining téyori ngenani [[molekul]] hépatotrofik ing portal [[pambuluh walik]] ing ati lan nemu [[hormon]] [[insulin]] minangka faktor hépatotrofik utama saka sapérangan faktor liya kang ana.<ref name="PM20235333">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/20235333
| title        = History of clinical transplantation.
| accessdate   = 2010-08-04
| work         = Thomas E. Starzl Transplantation Institute, University of Pittsburgh; Starzl TE
}}</ref> Ing wektu kang mèh bebarengan téyori ngenani transplantasi multiviseral lan ati uga ngrembaka saka studi [[imunosupresi]] kang nyinaoni algoritma empiris saka pangenalan pola lan rèspon térapis. Nalika awal 1960, dibuktèkaké yèn ''canine'' lan ''allograft'' manungsa nduwé toléransi kimersime kang bisa kaindhuksi otomatis kanthi bantuan imunosupresi, nganti akir 1962 disimpulaké kanthi klèru, yèn transplantasi nglibataké loro [[sistem kakebalan]] kang béda. Konsekwènsi kasimpulan mau dadi [[dogma]] yèn [[tolerogenisitas]] ati, dhasaré béda, ora mung karo sungsum balung mburi, nanging karo kabèh organ awak liyané.<ref name="PM11200418" /> Keklèron iki ora kakorèksi kanthi becik tekan taun 1990.<ref name="PM10833242" />

Transplantasi ati kang pisanan dilakokaké ing [[Denver]] nalika taun 1963,<ref name="PM12390423">{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/12390423
| title        = History of pediatric liver transplantation. Where are we coming from? Where do we stand?
| accessdate   = 2010-08-04
| work         = Department of Pediatric Surgery and Liver Transplantation, Université Catholique de Louvain; Otte JB.
}}</ref> pisanan kasil kacathet nalika taun 1967 kanthi [[azatioprina]], [[prednison]] lan [[globulin]] anti-limfoid, déning [[Thomas E. Starzl]] saka [[Amérikah Sarékat]], disusul déning kasilé transplantasi sungsum balung mburi manungsa nalika taun 1968.<ref name="PM10833242" /> Rentang wektu antara taun 1967 tekan 1979 nyathet kaping 84 transplantasi ati ing bocah kanthi 30% daya tahan urip tekan 2 taun.<ref name="PM12390423" />

Nrembakané studi imunosupresi banjur mènèhaké kabecikan lan pangarep-arep urip luwih dawa kanggo pasien, antarané kanthi panggantian azatioprina mawa [[siklosporina]] nalika taun 1979, banjur kagantèkaké mawa [[takrolimus]] nalika taun 1989.<ref name="PM20235333"/>

Nalika taun 1992, dikembangaké téyori [[Kimerisme#Mikrokimerisme|mikrokimerisme leukosit donor]]<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/16447295
| title        = The unfinished legacy of liver transplantation: emphasis on immunology.
| accessdate   = 2010-08-04
| work         = Transplantation Institute, Department of Surgery, University of Pittsburgh Medical Center; Starzl TE, Lakkis FG.
}}</ref> kanthi cakupan donor saka silsilah kang béda, kang mènèhaké pangarep-arep urip kang dawa banget kanggo panampa donor organ, sawisé dikawruhi gegandhèngan antarané aspèk imunologis saka transplantasi, [[infèksi]], toléransi déning [[sungsum balung mburi]], [[neoplasma]] lan kelainan otoimun, kang diarani [[mekanisme seminal]]. Rèspon kakebalan lan toléransi kakebalan antarané organ donor lan awak tinemu wujud fungsi saka migrasi lan lokalisasi [[leukosit]].<ref name="PM11200418" /> Salah siji temuané ya iku aktivasi [[sistem kakebalan turunan]] déning [[sèl NK]] lan [[interferon|interferon-γ]] langsung sawisé transplantasi rampung dilakokaké.<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/18292182
| title        = Activation of innate immunity (NK/IFN-gamma) in rat allogeneic liver transplantation: contribution to liver injury and suppression of hepatocyte proliferation
| accessdate   = 2010-08-04
| work         = Department of Hepatobiliary Surgery, First Affiliated Hospital, Zhejiang University School of Medicine; Shen K, Zheng SS, Park O, Wang H, Sun Z, Gao B.
}}</ref> Ing modhèl [[tikus]], sèl hépatosit donor tinemu asifat [[antigen]]ik banget saéngga njalari rèspon panulakan, kang bisa dilakokaké kanthi swatantra utawa bebarengan antarané [[sèl T CD4]] lan [[sèl T CD8]].<ref>{{cite web
| url          = http://www.ncbi.nlm.nih.gov/pubmed/10807522
| title        = Unusual patterns of alloimmunity evoked by allogeneic liver parenchymal cells.
| accessdate   = 2010-08-04
| work         = The Ohio State University College of Medicine, Department of Surgery; Bumgardner GL, Orosz CG.
}}</ref>

Kanggo iku diperlokaké [[terapi imunosupresif]] kang intensif sadurungé transplantasi dilakokaké, kang diarani ''preparative regimen'' utawa ''conditioning'' kanggo nyegah panulakan organ donor déning [[sistem kakebalan]] inang.<ref>{{cite book
| title = Holland-Frei Cancer medicine
| author = Kufe, Donald W.; Pollock, Raphael E.; Weichselbaum, Ralph R.; Bast, Robert C., Jr.; Gansler, Ted S.; Holland, James F.; Frei III, Emil.
| work    = Dana-Farber Cancer Institute, Harvard Medical School Boston, Department of Surgical Oncology, University of Texas, MD Anderson Cancer Center, Department of Radiation and Cellular Oncology, University of Chicago Hospital, Chicago Tumor Institute, University of Chicago Chicago, University of Texas, MD Anderson Cancer Center, Houston, American Cancer Society, Derald H Ruttenberg Cancer Center, Mount Sinai School of Medicine New York
| isbn = 1-55009-213-8
| edition = 6
| year = 2003
| page = Engraftment of Allogeneic Hematopoietic Transplants
| publisher = Hamilton on BC Decker Inc.,
| url = http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cmed6&part=A17328
| accessdate   = 2010-08-09
}}</ref> Terapi imunosupresif mau ditujokaké kanggo nekan [[sèl T]] lan [[sèl NK]] inang guna mènèhaké ruwang ing njero [[sungsum balung mburi]] kanggo transplantasi sèl punca hematopoietik saka organ donor liwat [[terapi mielosupresif]], kanggo kaseimbangan répopulasi sèl donor karo sèl asil diferensiasi saka sèl punca inang.

Diwasa iki, transplantasi ati dilakokaké mung nalika ati wis lumebu jenjang akir sawijining lelara, utawa wis dadi disfungsi akut kang diarani ''fulminant hepatic failure''. Kasus transplantasi ati ing manungsa lumrahé disebabaké déning [[sirosis ati]] akibat saka [[hépatitis C]] kronis, katergantungan alkohol, hepatitis otoimun lsp.

Tèknik umum kang dipigunakaké ya iku [[transplantasi ortotopik]], ya iku panempatan organ donor ing posisi anatomik kang padha karo posisi awal organ sadurungé. Transplantasi ati duwé potènsi bisa ditrepaké, mung yèn panampa organ donor ora duwé kaanan liya kang ngeboti, kaya ta [[kanker]] [[metastatis]] ing njaba organ ati, katergantungan marang usada utawa alkohol. Sapérangan ahli duwé pedoman ing [[kriteria Milan]] kanggo selèksi pasien transplantasi ati.

Organ donor, diarani ''allograft'', lumrahé asalé saka manungsa liya kang nembé nilar donya akibat tatu utek traumatik (kadaverik). Tèknik transplantasi liya migunakaké organ manungsa kang isih urip, oprasi [[hepatektomi]] ngangkat 20% ati ing sègmèn Coinaud 2 lan 3 saka wong diwasa kanggo didonoraké marang sawijining bocah, nalika taun 1989.

== Wacan terusan ==
* [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1180834/table/T6] Èksprèsi genetik kang diindhuksi déning [[hormon]] [[tri-iodotironina]] lan [[hormon pertumbuhan|GH]]

== Rujukan ==
{{Reflist|colwidth=30em}}

== Pranala njaba ==
{{commons|Category:Liver}}
* [http://www.aasld.org American Association for the Study of Liver Diseases] AASLD
* [http://www.liversociety.org American Liver Society] {{Webarchive|url=https://web.archive.org/web/20160112044212/http://www.liversociety.org/ |date=2016-01-12 }} ALS
* [http://mathis.heydtmann.de/WikiLiver WikiLiver: A Wiki dedicated to the liver]

{{sistem pancernan}}

[[Kategori:Sistem pancernan]]
[[Kategori:Organ]]
[[Kategori:Abdomen]]