Nekrosis

Nekrosis inggih punika satunggaling wujud cidera sel ingkang nyebabaken pejahipun sel kanthi prematur wonten ing jaringan urip amargi autolisis.^[1] Istilah "nekrosis" dipunwiwiti wonten ing pertengahan abad kaping-19 lan asring dipunhubungaken kaliyan ahli patologi Jerman Rudolf Virchow, ingkang asring dipunanggep minangka salah satunggaling pendiri patologi modern.^[2] Nekrosis dipunsebabaken dening faktor-faktor eksternal tumrap sel utawi jaringan, kadosta infeksi, utawi trauma ingkang nyebabaken pencernaan komponen sel ingkang boten diatur. Kosokwangsulipun, apoptosis inggih punika penyebab kematian sel ingkang dipunprogram lan dipuntargetaken kanthi alami. Sinaosa apoptosis asring maringi efek ingkang migunani tumrap organisme, nekrosis meh tansah mbebayani lan saged mbebayani jiwa.^[3]

Pejahipun sel amargi nekrosis boten nderek poros transduksi sinyal apoptotik, nanging maneka warni reseptor dipunaktifaken lan nyebabaken risaking integritas membran sel^[4] lan medalipun produk kematian sel ingkang boten dipunkontrol dhateng ruang ekstrasellular.^[1] Punika miwiti respons peradangan ing jaringan sakiwa tengenipun, ingkang narik leukosit lan fagosit ingkang celak ingkang ngicali sel-sel ingkang pejah kanthi fagositosis. Nanging, zat ingkang ngrusak mikroba ingkang dipunbebas dening leukosit saged ndamel kerusakan kolateral dhateng jaringan sakiwa tengenipun.^[5] Kerusakan kolateral ingkang ageng punika ngalang-alangi proses panyembuhan. Kanthi mekaten, nekrosis ingkang boten dipunobati nyebabaken akumulasi jaringan pejah ingkang sami rusak lan reruntuhan sel wonten ing utawi celak papan kematian sel. Satunggaling tuladha klasik inggih punika gangren. Amargi alesan punika, asring kersa ngicali jaringan nekrotik kanthi operasi, prosedur ingkang dipunsebat debridement.

Sitiran

↑ ^a ^b Proskuryakov SY, Konoplyannikov AG, Gabai VL (February 2003). "Necrosis: a specific form of programmed cell death?". Experimental Cell Research. 283 (1): 1–16. doi:10.1016/S0014-4827(02)00027-7. PMID 12565815.
↑ Gerschenson, L.E.; Geske, F. Jon (April 2001). "Virchow and Apoptosis". The American Journal of Pathology (ing basa Inggris). 158 (4): 1543. doi:10.1016/S0002-9440(10)64105-3. PMC 1891904. PMID 11290572.
↑ Kasper DL, Zaleznik DF (2001). "Gas gangrene, antibiotic associated colitis, and other Clostridial infections". Ing Stone RM (èd.). Harrison's principles of internal medicine self-assessment and board review (édhisi ka-15th). New York: McGraw-Hill, Medical Pub. Division. kc. 922–927. ISBN 978-0071386784.
↑ Nirmala JG, Lopus M (April 2020). "Cell death mechanisms in eukaryotes". Cell Biology and Toxicology. 36 (2): 145–164. doi:10.1007/s10565-019-09496-2. PMID 31820165. S2CID 208869679.
↑ Rock KL, Kono H (2008). "The inflammatory response to cell death". Annual Review of Pathology. 3: 99–126. doi:10.1146/annurev.pathmechdis.3.121806.151456. PMC 3094097. PMID 18039143.

[Proskuryakov-1] Proskuryakov SY, Konoplyannikov AG, Gabai VL (February 2003). "Necrosis: a specific form of programmed cell death?". Experimental Cell Research. 283 (1): 1–16. doi:10.1016/S0014-4827(02)00027-7. PMID 12565815.

[2] Gerschenson, L.E.; Geske, F. Jon (April 2001). "Virchow and Apoptosis". The American Journal of Pathology (ing basa Inggris). 158 (4): 1543. doi:10.1016/S0002-9440(10)64105-3. PMC 1891904. PMID 11290572.

[Kasper-3] Kasper DL, Zaleznik DF (2001). "Gas gangrene, antibiotic associated colitis, and other Clostridial infections". Ing Stone RM (èd.). Harrison's principles of internal medicine self-assessment and board review (édhisi ka-15th). New York: McGraw-Hill, Medical Pub. Division. kc. 922–927. ISBN 978-0071386784.

[4] Nirmala JG, Lopus M (April 2020). "Cell death mechanisms in eukaryotes". Cell Biology and Toxicology. 36 (2): 145–164. doi:10.1007/s10565-019-09496-2. PMID 31820165. S2CID 208869679.

[5] Rock KL, Kono H (2008). "The inflammatory response to cell death". Annual Review of Pathology. 3: 99–126. doi:10.1146/annurev.pathmechdis.3.121806.151456. PMC 3094097. PMID 18039143.

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