摘要
细胞坏死和凋亡是导致缺血再灌注损伤(ischemia-reperfusion injury,IRI)的主要原因,最新研究表明一种新的细胞死亡方式—坏死性凋亡(necroptosis)也参与其中。坏死性凋亡兼具凋亡和坏死的特征,遗憾的是其分子机制尚未完全明确。本文总结了在各类组织脏器发生IRI后,可以通过抑制坏死性凋亡来降低这种损伤的作用靶点。
Cell necrosis and apoptosis are the main causes of ischemia-reperfusion injury (IRI), and the latest research shows that a new way of cell death, necroptosis, is also involved. Necroptosis has the characteristics of apoptosis and necrosis. However, its molecular mechanism is not completely clear. This paper summarizes the various targets which can reduce the injury by inhibiting necroptosis after IRI.
作者
徐佳
陈桂浩
孙林
杨跃进
XU Jia;CHEN Gui-hao;SUN Lin;YANG Yue-jin(Department of Cardiology,Second Affiliated Hospital of Kunming Medical University,Kunming 650101,Yunnan;Fuwai Hospital,Chinese Academy of Medical Sciences,Beijing 100037,China)
出处
《中国分子心脏病学杂志》
CAS
2019年第1期2778-2780,共3页
Molecular Cardiology of China
基金
国家自然科学基金(81560050)
云南省科技厅联合专项--昆明医科大学基金(2014FB047)
