文章摘要

细胞程序性坏死及其在炎症中的作用

作者: 1,2易翼虎, 2左笑丛
1 中南大学湘雅医学院，长沙 410013
2 中南大学湘雅三医院药学部，长沙 410013
通讯: 左笑丛 Email: zuoxc08@126.com
DOI: 10.3978/j.issn.2095-6959.2016.11.037
基金: 中南大学湘雅三医院“新湘雅人才工程至善领跑计划”, 20150218 新世纪优秀人才支持计划, NCET-13-0605

摘要

可调节性细胞死亡在组织稳态中发挥至关重要的作用。最新发现：程序性坏死作为一种调节途径，其涉及RIPK3和MLKL蛋白的参与，且由死亡受体、干扰素、Toll样受体、细胞内RNA和DNA感应器体或其他介质诱发。RIPK1具有激酶依赖性支架功能，可抑制或激发细胞坏死和凋亡。小鼠模型研究显示了程序性坏死在炎症中所发挥的重要作用，这对于研究许多人类的炎性疾病发病原理有重要意义。本文讨论了程序性坏死调节机制及其在炎症和疾病中发挥的潜在作用。
关键词： 程序性坏死 可调节性细胞死亡 炎症

Necroptosis and its role in inflammation

Authors: 1,2YI Yihu, 2ZUO Xiaocong
1 School of Xiangya Medical Science of Central South University, Changsha 410013
2 Clinical Pharmacy and Pharmacology Research Institute, The Third Xiangya Hospital of Central South University, Changsha 410013, China

CorrespondingAuthor: ZUO Xiaocong Email: zuoxc08@126.com

DOI: 10.3978/j.issn.2095-6959.2016.11.037

Abstract

Regulated cell death has essential functions in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.

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