程序性细胞坏死的分子机制及其在炎症中的作用

发布时间：2018-04-12 07:37

本文选题：程序性细胞坏死 + 激酶　；参考：《中国细胞生物学学报》2016年01期

【摘要】：越来越多的研究表明,细胞坏死是一种受到精密调控的"新型"程序性细胞死亡方式。当细胞凋亡不能正常发生而细胞必须死亡时,坏死作为凋亡的"替补"方式被激活。程序性细胞坏死主要由肿瘤坏死因子受体(tumor necrosis factor receptor,TNFR)家族以及Toll样受体(Toll-like receptor,TLR)家族启动,并通过和受体蛋白互作的两个蛋白激酶RIP1(receptor interacting protein kinase 1)和RIP3(receptor interacting protein kinase 3)传递死亡信号,募集并磷酸化MLKL(mixed lineage kinase domain-like protein),而MLKL作为细胞死亡的执行者最终会导致坏死的发生。坏死的细胞会向周围释放其内容物,这些内容物作为DAMPs(damage-associated molecular pattern molecules)可刺激周围细胞发生炎症反应,激活机体免疫应答。该文以TNF-α诱导的细胞坏死途径为出发点,着重阐述程序性细胞坏死的分子机制及其在炎症中的作用,并回顾和展望了其在临床诊疗中的可能性。
[Abstract]:More and more studies show that cell necrosis is a kind of "new" by the precise regulation of programmed cell death. Apoptosis can occur when normal cells must be activated as death, necrosis and apoptosis of "substitute". Programmed cell necrosis mainly by tumor necrosis factor receptor (tumor necrosis factor receptor. TNFR) family and Toll like receptor (Toll-like receptor TLR) family started, two protein kinase RIP1 and the receptor protein interaction (receptor interacting protein kinase 1) and RIP3 (receptor interacting protein kinase 3) transmit death signal, recruitment and phosphorylation of MLKL (mixed lineage kinase domain-like protein), and MLKL as the executor of cell death eventually lead to necrosis. Necrosis of the cells will release its contents into the surrounding, the content of DAMPs (damage-associated as mole Cular pattern molecules) can stimulate the peripheral cell inflammation, activate the immune response. In this paper, way of cell necrosis induced by TNF- as a starting point, focuses on the molecular mechanisms of programmed cell necrosis and its role in inflammation, and discussed its possibility in the clinical diagnosis and treatment and review.

【作者单位】：细胞生物学国家重点实验室中国科学院上海生命科学研究院生物化学与细胞生物学研究所;
【基金】：国家自然科学基金(批准号:31471302)资助的课题~~
【分类号】：R363

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