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Mitochondrial dysfunction in cell senescence and aging

delete2022-07-01
delete367
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OA
AI
S
Satomi Miwa
S
Sonu Kashyap
E
Eduardo N. Chini
T
Thomas von Zglinicki *
DOI:10.1172/JCI158447delete
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摘要

摘要

En 中文
Mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely interconnected. Mitochondrial dysfunction, operationally defined as a decreased respiratory capacity per mitochondrion together with a decreased mitochondrial membrane potential, typically accompanied by increased production of oxygen free radicals, is a cause and a consequence of cellular senescence and figures prominently in multiple feedback loops that induce and maintain the senescent phenotype. Here, we summarize pathways that cause mitochondrial dysfunction in senescence and aging and discuss the major consequences of mitochondrial dysfunction and how these consequences contribute to senescence and aging. We also highlight the potential of senescence-associated mitochondrial dysfunction as an antiaging and antisenescence intervention target, proposing the combination of multiple interventions converging onto mitochondrial dysfunction as novel, potent senolytics.
Keyword:
DNA-DAMAGE RESPONSE
OXIDATIVE STRESS
SECRETORY PHENOTYPE
CALCIUM REGULATION
MTDNA MUTATIONS
NAD(+)
ROS
AGE
INFLAMMATION
ACTIVATION
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期刊

Journal of Clinical Investigation 封面图
Journal of Clinical Investigation
IF:
13.6
论文数:
1.5W
被引数:
11.5W

机构

N
newcastle university - uk
学者数:
2.9W
论文数: 2.6W
被引数: 39
M
mayo clinic
学者数:
8.3W
论文数: 6.6W
被引数: 85
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