生命科学研究2026，Vol.30Issue(2)：95-108,14.DOI:10.16605/j.cnki.1007-7847.2025.09.0182
程序性细胞坏死:从分子机制到疾病
Necroptosis:From Molecular Mechanisms to Diseases
摘要
Abstract
Necroptosis is a cysteinyl aspartate specific proteinase(caspase)-independent form of programmed cell death mediated by death receptors and executed by the mixed lineage kinase domain-like protein(MLKL),which exhibits typical morphological features of necrosis.The core signaling pathway of necroptosis is initiated by the activation of signals such as death receptors.Key steps include the complex formation of receptor-interacting protein kinase 1(RIPK1)and RIPK3,which subsequently recruits and phosphorylates the downstream effector MLKL,ultimately leading to plasma membrane rupture.Activated MLKL undergoes oligomerization and translocates to the plasma membrane,where it disrupts membrane integrity either by di-rect pore formation or indirect regulation of ion channels,resulting in intracellular content leakage and in-flammatory responses.Substantial evidence indicates that dysregulated necroptosis is closely associated with the pathophysiology of various human diseases,including inflammatory disorders,immune-related conditions,degenerative diseases,and cancer.This review aims to summarize the core molecular mechanisms and sig-naling networks of necroptosis,as well as its roles in related diseases,thereby providing a theoretical founda-tion for developing therapeutic strategies targeting this pathway.关键词
程序性细胞坏死/炎症/人类疾病/分子机制/治疗策略Key words
necroptosis/inflammation/human disease/molecular mechanism/therapeutic strategy分类
生物科学引用本文复制引用
宋新刚,宋国荣,段云蔚,蒲燕珍,陈浩杰,贺源,蔡振宇,郭瑜峰..程序性细胞坏死:从分子机制到疾病[J].生命科学研究,2026,30(2):95-108,14.基金项目
国家自然科学基金面上项目(32170748) （32170748）
国网上海市电力公司科技项目(520900220007) （520900220007）
