自噬
程序性细胞死亡
坏死
细胞凋亡
缺血
医学
发病机制
心肌梗塞
心力衰竭
细胞
机制(生物学)
心肌细胞
疾病
心肌细胞
生物
细胞生物学
免疫学
心脏病学
病理
遗传学
哲学
认识论
作者
Russell S. Whelan,Vladimir Kaplinskiy,Richard N. Kitsis
出处
期刊:Annual Review of Physiology
[Annual Reviews]
日期:2010-03-17
卷期号:72 (1): 19-44
被引量:649
标识
DOI:10.1146/annurev.physiol.010908.163111
摘要
Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.
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