生物
线粒体
细胞生物学
线粒体DNA
重编程
氧化磷酸化
细胞器
线粒体生物发生
功能(生物学)
线粒体融合
逆行信号
信号转导
细胞器生物发生
氧化损伤
氧化应激
遗传学
生物发生
内分泌学
基因
生物化学
作者
G. R. Scott Budinger,Navdeep S. Chandel
出处
期刊:Genes & Development
[Cold Spring Harbor Laboratory Press]
日期:2025-07-11
卷期号:39 (15-16): 917-919
被引量:1
标识
DOI:10.1101/gad.353106.125
摘要
Mitochondria are no longer viewed solely as ATP- or metabolite-generating organelles but as key regulators of cellular signaling that shape physiologic aging. Contrary to earlier theories linking aging to mitochondrial DNA mutations and oxidative damage, current evidence shows that these factors do not causally limit physiologic aging. Instead, an evolving literature links age-related loss of mitochondrial signaling and function to important physiologic changes of aging. Moreover, mild inhibition of mitochondrial respiratory function with drugs like metformin promote health span. These findings open new paths for pharmacologically reprogramming mitochondrial signaling to extend healthy aging.
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