粒体自噬
自噬
线粒体
线粒体融合
衰老
生物
细胞生物学
心力衰竭
线粒体生物发生
调节器
线粒体分裂
神经科学
生物信息学
医学
细胞凋亡
内科学
线粒体DNA
遗传学
基因
作者
Agnieszka Biala,Rimpy Dhingra,Lorrie A. Kirshenbaum
标识
DOI:10.1016/j.yjmcc.2015.04.015
摘要
Aging is a degenerative process that unfortunately is an inevitable part of life and risk factor for cardiovascular disease including heart failure. Among the several theories purported to explain the effects of age on cardiac dysfunction, the mitochondrion has emerged a central regulator of this process. Hence, it is not surprising that abnormalities in mitochondrial quality control including biogenesis and turnover have such detrimental effects on cardiac function. In fact mitochondria serve as a conduit for biological signals for apoptosis, necrosis and autophagy respectively. The removal of damaged mitochondria by autophagy/mitophagy is essential for mitochondrial quality control and cardiac homeostasis. Defects in mitochondrial dynamism fission/fusion events have been linked to cardiac senescence and heart failure. In this review we discuss the impact of aging on mitochondrial dynamics and senescence on cardiovascular health. This article is part of a Special Issue entitled: CV Aging.
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