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Mitochondrial dysfunction in cell senescence and aging

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 p...

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Detalles Bibliográficos
Autores principales: Miwa, Satomi, Kashyap, Sonu, Chini, Eduardo, von Zglinicki, Thomas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Clinical Investigation 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9246372/
https://www.ncbi.nlm.nih.gov/pubmed/35775483
http://dx.doi.org/10.1172/JCI158447
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author Miwa, Satomi
Kashyap, Sonu
Chini, Eduardo
von Zglinicki, Thomas
author_facet Miwa, Satomi
Kashyap, Sonu
Chini, Eduardo
von Zglinicki, Thomas
author_sort Miwa, Satomi
collection PubMed
description 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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spelling pubmed-92463722022-07-02 Mitochondrial dysfunction in cell senescence and aging Miwa, Satomi Kashyap, Sonu Chini, Eduardo von Zglinicki, Thomas J Clin Invest Review Series 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. American Society for Clinical Investigation 2022-07-01 2022-07-01 /pmc/articles/PMC9246372/ /pubmed/35775483 http://dx.doi.org/10.1172/JCI158447 Text en © 2022 Miwa et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review Series
Miwa, Satomi
Kashyap, Sonu
Chini, Eduardo
von Zglinicki, Thomas
Mitochondrial dysfunction in cell senescence and aging
title Mitochondrial dysfunction in cell senescence and aging
title_full Mitochondrial dysfunction in cell senescence and aging
title_fullStr Mitochondrial dysfunction in cell senescence and aging
title_full_unstemmed Mitochondrial dysfunction in cell senescence and aging
title_short Mitochondrial dysfunction in cell senescence and aging
title_sort mitochondrial dysfunction in cell senescence and aging
topic Review Series
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9246372/
https://www.ncbi.nlm.nih.gov/pubmed/35775483
http://dx.doi.org/10.1172/JCI158447
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