Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 132, Issue 13, Pages -Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI158447
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Funding
- Cancer Research United Kingdom [C12161/A24009]
- Biotechnology and Biological Sciences Research Council [BB/S006710/1]
- Innovate United Kingdom [11272]
- Medical Research Council (MRC) Versus Arthritis Centre for Integrated Research into Musculoskeletal Ageing grant
- UK SPINE grant [B06]
- H2020 WIDESPREAD [857524]
- Ted Nash Long Life Foundation
- Glenn Foundation for Medical Research via the Paul F. Glenn Laboratories for the Biology of Aging
- Mayo Foundation
- Noaber Foundation
- Calico Life Sciences LLC
- NIH National Institute on Aging [AG26094, AG58812, CA233790]
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This article summarizes the importance of mitochondrial dysfunction in aging and cell senescence, discusses its relationship with cellular senescence, and proposes an anti-aging therapy that targets mitochondrial dysfunction.
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.
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