衰老
线粒体
细胞生物学
氧化磷酸化
生物
活性氧
重编程
线粒体ROS
氧化应激
线粒体DNA
生物化学
细胞
基因
作者
Yun Haeng Lee,Ji Yun Park,Haneur Lee,Eun Seon Song,Myeong Uk Kuk,Junghyun Joo,Seajin Oh,Hyung-Wook Kwon,Taezoon Park,Sang Chul Park
出处
期刊:Cells
[MDPI AG]
日期:2021-11-03
卷期号:10 (11): 3003-3003
被引量:20
标识
DOI:10.3390/cells10113003
摘要
Mitochondria are one of organelles that undergo significant changes associated with senescence. An increase in mitochondrial size is observed in senescent cells, and this increase is ascribed to the accumulation of dysfunctional mitochondria that generate excessive reactive oxygen species (ROS). Such dysfunctional mitochondria are prime targets for ROS-induced damage, which leads to the deterioration of oxidative phosphorylation and increased dependence on glycolysis as an energy source. Based on findings indicating that senescent cells exhibit mitochondrial metabolic alterations, a strategy to induce mitochondrial metabolic reprogramming has been proposed to treat aging and age-related diseases. In this review, we discuss senescence-related mitochondrial changes and consequent mitochondrial metabolic alterations. We assess the significance of mitochondrial metabolic reprogramming for senescence regulation and propose the appropriate control of mitochondrial metabolism to ameliorate senescence. Learning how to regulate mitochondrial metabolism will provide knowledge for the control of aging and age-related pathologies. Further research focusing on mitochondrial metabolic reprogramming will be an important guide for the development of anti-aging therapies, and will provide novel strategies for anti-aging interventions.
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