粒体自噬
自噬
线粒体
长寿
生物
细胞生物学
生物能学
机制(生物学)
帕金
衰老
神经科学
帕金森病
疾病
遗传学
医学
细胞凋亡
病理
哲学
认识论
作者
Jing Guo,Wei Chung Chiang
出处
期刊:Iubmb Life
[Wiley]
日期:2021-12-10
卷期号:74 (4): 296-316
被引量:11
摘要
The clearance of damaged or unwanted mitochondria by autophagy (also known as mitophagy) is a mitochondrial quality control mechanism postulated to play an essential role in cellular homeostasis, metabolism, and development and confers protection against a wide range of diseases. Proper removal of damaged or unwanted mitochondria is essential for organismal health. Defects in mitophagy are associated with Parkinson's, Alzheimer's disease, cancer, and other degenerative disorders. Mitochondria regulate organismal fitness and longevity via multiple pathways, including cellular senescence, stem cell function, inflammation, mitochondrial unfolded protein response (mtUPR), and bioenergetics. Thus, mitophagy is postulated to be pivotal for maintaining organismal healthspan and lifespan and the protection against aged-related degeneration. In this review, we will summarize recent understanding of the mechanism of mitophagy and aspects of mitochondrial functions. We will focus on mitochondria-related cellular processes that are linked to aging and examine current genetic evidence that supports the hypothesis that mitophagy is a pro-longevity mechanism.
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