Necroptosis的调控机制及其在组织及细胞缺血损伤中的作用和意义  

Regulatory Mechanism and Important Role of Necroptosis in Tissue and Cell Ischemic Injury

作　　者：于光耀[1] 贾彩云[1] 马远方[1] 

机构地区：[1]河南大学医学院免疫学研究所,河南省开封市475004

出　　处：《医学分子生物学杂志》2009年第6期547-549,共3页Journal of Medical Molecular Biology

基　　金：资助项目：河南省杰出人才创新基金（No.074200510014）

摘　　要：Necroptosis不同于坏死和凋亡，具有坏死的细胞形态特点和自噬的活化，并且是主动耗能的，是被一系列信号传导通路所调控的细胞死亡机制。Necroptosis的发现和确认为细胞死亡的逆转和治疗开创了一个新的研究和应用途经。RIPl激酶是调控Necroptosis形成的关键酶，Necrostatins则是一类小分子化合物，它通过特异性地抑制细胞RIPl激酶而抑制Necroptosis的形成。Necroptosis is different from necrosis and apoptosis and characterized by necrotic cell death morphology and activation of autophagy. Necroptosis is an active and energy consuming cell death mechanism, which is regulated by a set of signal-transduction pathways. The discovery and i- dentification of necroptosis has initiated a new approach of research and application for cell death re- version and treatment. RIP1 kinase has been identified as a key enzyme to regulate necropto- sis. Necrostatins are one kind of small molecule compounds that specifically block the execution of necroptosis by inhibiting RIP1 kinase activity. In this review, we elucidate the execution and regula- tion of tissue and cell necroptosis from gene level, cellular level to animal models, to provide com- prehensive information and understanding of necroptosis.

关 键 词：坏死状凋亡 RIPI Necrostatins 组织缺血损伤 

分 类 号：Q255[生物学—细胞生物学]