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Changes in Redox Signaling in the Skeletal Muscle with Aging

Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfuncti...

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Autores principales: Szentesi, Péter, Csernoch, László, Dux, László, Keller-Pintér, Anikó
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6360032/
https://www.ncbi.nlm.nih.gov/pubmed/30800208
http://dx.doi.org/10.1155/2019/4617801
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author Szentesi, Péter
Csernoch, László
Dux, László
Keller-Pintér, Anikó
author_facet Szentesi, Péter
Csernoch, László
Dux, László
Keller-Pintér, Anikó
author_sort Szentesi, Péter
collection PubMed
description Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfunction and increased oxidative stress are the central driving forces for age-related skeletal muscle abnormalities. The increased oxidative stress in the aged muscle can lead to altered excitation-contraction coupling and calcium homeostasis. Furthermore, apoptosis-mediated fiber loss, atrophy of the remaining fibers, dysfunction of the satellite cells (muscle stem cells), and concomitant impaired muscle regeneration are also the consequences of increased oxidative stress, leading to a decrease in muscle mass, strength, and function of the aged muscle. Here we summarize the possible effects of oxidative stress in the aged muscle and the benefits of physical activity and antioxidant therapy.
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spelling pubmed-63600322019-02-24 Changes in Redox Signaling in the Skeletal Muscle with Aging Szentesi, Péter Csernoch, László Dux, László Keller-Pintér, Anikó Oxid Med Cell Longev Review Article Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfunction and increased oxidative stress are the central driving forces for age-related skeletal muscle abnormalities. The increased oxidative stress in the aged muscle can lead to altered excitation-contraction coupling and calcium homeostasis. Furthermore, apoptosis-mediated fiber loss, atrophy of the remaining fibers, dysfunction of the satellite cells (muscle stem cells), and concomitant impaired muscle regeneration are also the consequences of increased oxidative stress, leading to a decrease in muscle mass, strength, and function of the aged muscle. Here we summarize the possible effects of oxidative stress in the aged muscle and the benefits of physical activity and antioxidant therapy. Hindawi 2019-01-17 /pmc/articles/PMC6360032/ /pubmed/30800208 http://dx.doi.org/10.1155/2019/4617801 Text en Copyright © 2019 Péter Szentesi et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Szentesi, Péter
Csernoch, László
Dux, László
Keller-Pintér, Anikó
Changes in Redox Signaling in the Skeletal Muscle with Aging
title Changes in Redox Signaling in the Skeletal Muscle with Aging
title_full Changes in Redox Signaling in the Skeletal Muscle with Aging
title_fullStr Changes in Redox Signaling in the Skeletal Muscle with Aging
title_full_unstemmed Changes in Redox Signaling in the Skeletal Muscle with Aging
title_short Changes in Redox Signaling in the Skeletal Muscle with Aging
title_sort changes in redox signaling in the skeletal muscle with aging
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6360032/
https://www.ncbi.nlm.nih.gov/pubmed/30800208
http://dx.doi.org/10.1155/2019/4617801
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