细胞死亡在心脏病发病机制中的作用:机制和意义。

Cell death in the pathogenesis of heart disease: mechanisms and significance.

机构信息

Wilf Family Cardiovascular Research Institute and the Departments of Medicine and Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

出版信息

Annu Rev Physiol. 2010;72:19-44. doi: 10.1146/annurev.physiol.010908.163111.

Abstract

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.

摘要

细胞死亡曾经被认为是不受调控的。现在很清楚,至少一部分细胞死亡是一种受调控的细胞自杀过程。这种死亡方式可以表现出多种形态。其中一种,凋亡,长期以来一直被认为是主动介导的,其许多潜在机制已经被阐明。此外,坏死,传统的不受调控的细胞死亡的例子,在某些情况下也是受调控的。自噬通常是一种生存机制,但也可能与细胞死亡有关。然而,关于自噬细胞如何死亡,我们知之甚少。在心肌梗死、缺血/再灌注和心力衰竭期间,凋亡、坏死和自噬发生在心肌细胞中。在这些疾病中,凋亡和坏死的药理学和遗传学抑制可减少梗死面积并改善心功能。自噬在缺血/再灌注和心力衰竭中的作用仍未解决。更好地了解这些过程及其相互关系,可能为主要心脏综合征的新型治疗方法的发展提供依据。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索