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Mitochondria and Organismal Longevity

Mitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-depen...

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Detalles Bibliográficos
Autores principales: Hwang, Ara B, Jeong, Dae-Eun, Lee, Seung-Jae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468885/
https://www.ncbi.nlm.nih.gov/pubmed/23633912
http://dx.doi.org/10.2174/138920212803251427
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author Hwang, Ara B
Jeong, Dae-Eun
Lee, Seung-Jae
author_facet Hwang, Ara B
Jeong, Dae-Eun
Lee, Seung-Jae
author_sort Hwang, Ara B
collection PubMed
description Mitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-dependent decline in biological function. However, recent studies show that increased levels of ROS or inhibition of mitochondrial function can actually delay aging and increase lifespan. The aim of this review is to summarize recent findings regarding the role of mitochondria in organismal aging processes. We will discuss how mitochondria contribute to evolutionarily conserved longevity pathways, including mild inhibition of respiration, dietary restriction, and target of rapamycin (TOR) signaling.
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spelling pubmed-34688852013-05-01 Mitochondria and Organismal Longevity Hwang, Ara B Jeong, Dae-Eun Lee, Seung-Jae Curr Genomics Article Mitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-dependent decline in biological function. However, recent studies show that increased levels of ROS or inhibition of mitochondrial function can actually delay aging and increase lifespan. The aim of this review is to summarize recent findings regarding the role of mitochondria in organismal aging processes. We will discuss how mitochondria contribute to evolutionarily conserved longevity pathways, including mild inhibition of respiration, dietary restriction, and target of rapamycin (TOR) signaling. Bentham Science Publishers 2012-11 2012-11 /pmc/articles/PMC3468885/ /pubmed/23633912 http://dx.doi.org/10.2174/138920212803251427 Text en ©2012 Bentham Science Publishers http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Article
Hwang, Ara B
Jeong, Dae-Eun
Lee, Seung-Jae
Mitochondria and Organismal Longevity
title Mitochondria and Organismal Longevity
title_full Mitochondria and Organismal Longevity
title_fullStr Mitochondria and Organismal Longevity
title_full_unstemmed Mitochondria and Organismal Longevity
title_short Mitochondria and Organismal Longevity
title_sort mitochondria and organismal longevity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468885/
https://www.ncbi.nlm.nih.gov/pubmed/23633912
http://dx.doi.org/10.2174/138920212803251427
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