摘要
受体相互作用蛋白（RIP）是细胞坏死性凋亡中的关键因子，在创伤、缺血／再灌注（I／R）损伤及全身炎症反应综合征（SIRS）等过程中具有致炎作用。RIPl是坏死性凋亡小体（Ripoptosome）的主要成分，而Ripoptosome是调节细胞凋亡或坏死性凋亡形式的复合体。从RIP依赖的细胞死亡及炎症反应等分子机制人手，通过总结RIP介导凋亡、坏死性凋亡及炎症反应的机制，发现RIP位于凋亡、坏死性凋亡及炎症反应的网络信号调控的中心环节。因此，深入研究RIP介导的坏死性凋亡，将为I／R损伤、创伤、SIRS及肿瘤等多种疾病的治疗提供新的治疗靶点。
The receptor-interacting protein （RIP） has been identified to play a critical role in necroptosis, which is an inflammatory form of programmed necrosis in traμma, isehemia/reperfusion （I/R）, and systemic inflammatory response syndrome （SIRS）. Ripoptosome, a newly defined intracellular signaling complex with essential molecule of RIP1, can switch cell death mode between apoptosis and necroptosis. Based on molecular mechanism of RIP-dependent cell death and inflammation, with the understanding of the mechanisms of RIP-dependent apoptosis/neeroptosis and its role in inflammation was sμmmed up, and it was found that RIP plays a crucial role in regulating programmed cell death and inflammation. Therefore, further advances in understanding the mechanisms of necroptosis would be important in order to manipulate programmed cell death for therapeutic purposes in I/R injury, traμma, SIRS, and tμmor.
出处
《中华危重病急救医学》
CAS
CSCD
北大核心
2016年第2期184-187,共4页
Chinese Critical Care Medicine
基金
上海市科技发展基金（14411971100）
上海市青年医师培养资助计划项目（2012-114）
