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Cardiovascular aging: the mitochondrial influence

Age-associated cardiovascular disease is becoming progressively prevalent due to the increased lifespan of the population. However, the fundamental mechanisms underlying the aging process and the corresponding decline in tissue functions are still poorly understood. The heart has a very high energy...

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Autores principales: Sagar, Shakti, Gustafsson, Asa B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10426788/
https://www.ncbi.nlm.nih.gov/pubmed/37583788
http://dx.doi.org/10.20517/jca.2023.22
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author Sagar, Shakti
Gustafsson, Asa B.
author_facet Sagar, Shakti
Gustafsson, Asa B.
author_sort Sagar, Shakti
collection PubMed
description Age-associated cardiovascular disease is becoming progressively prevalent due to the increased lifespan of the population. However, the fundamental mechanisms underlying the aging process and the corresponding decline in tissue functions are still poorly understood. The heart has a very high energy demand and the cellular energy needed to sustain contraction is primarily generated by mitochondrial oxidative phosphorylation. Mitochondria are also involved in supporting various metabolic processes, as well as activation of the innate immune response and cell death pathways. Given the central role of mitochondria in energy metabolism and cell survival, the heart is highly susceptible to the effects of mitochondrial dysfunction. These key organelles have been implicated as underlying drivers of cardiac aging. Here, we review the evidence demonstrating the mitochondrial contribution to the cardiac aging process and disease susceptibility. We also discuss the potential mechanisms responsible for the age-related decline in mitochondrial function.
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spelling pubmed-104267882023-08-15 Cardiovascular aging: the mitochondrial influence Sagar, Shakti Gustafsson, Asa B. J Cardiovasc Aging Article Age-associated cardiovascular disease is becoming progressively prevalent due to the increased lifespan of the population. However, the fundamental mechanisms underlying the aging process and the corresponding decline in tissue functions are still poorly understood. The heart has a very high energy demand and the cellular energy needed to sustain contraction is primarily generated by mitochondrial oxidative phosphorylation. Mitochondria are also involved in supporting various metabolic processes, as well as activation of the innate immune response and cell death pathways. Given the central role of mitochondria in energy metabolism and cell survival, the heart is highly susceptible to the effects of mitochondrial dysfunction. These key organelles have been implicated as underlying drivers of cardiac aging. Here, we review the evidence demonstrating the mitochondrial contribution to the cardiac aging process and disease susceptibility. We also discuss the potential mechanisms responsible for the age-related decline in mitochondrial function. 2023-07 2023-07-17 /pmc/articles/PMC10426788/ /pubmed/37583788 http://dx.doi.org/10.20517/jca.2023.22 Text en https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Article
Sagar, Shakti
Gustafsson, Asa B.
Cardiovascular aging: the mitochondrial influence
title Cardiovascular aging: the mitochondrial influence
title_full Cardiovascular aging: the mitochondrial influence
title_fullStr Cardiovascular aging: the mitochondrial influence
title_full_unstemmed Cardiovascular aging: the mitochondrial influence
title_short Cardiovascular aging: the mitochondrial influence
title_sort cardiovascular aging: the mitochondrial influence
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10426788/
https://www.ncbi.nlm.nih.gov/pubmed/37583788
http://dx.doi.org/10.20517/jca.2023.22
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