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Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies

Oxidative stress is a loss of balance between the production of reactive oxygen species during cellular metabolism and the mechanisms that clear these species to maintain cellular redox homeostasis. Increased oxidative stress has been associated with muscular dystrophy, and many studies have propose...

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Detalles Bibliográficos
Autores principales: Choi, Min Hee, Ow, Jin Rong, Yang, Nai-Di, Taneja, Reshma
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700198/
https://www.ncbi.nlm.nih.gov/pubmed/26798425
http://dx.doi.org/10.1155/2016/6842568
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author Choi, Min Hee
Ow, Jin Rong
Yang, Nai-Di
Taneja, Reshma
author_facet Choi, Min Hee
Ow, Jin Rong
Yang, Nai-Di
Taneja, Reshma
author_sort Choi, Min Hee
collection PubMed
description Oxidative stress is a loss of balance between the production of reactive oxygen species during cellular metabolism and the mechanisms that clear these species to maintain cellular redox homeostasis. Increased oxidative stress has been associated with muscular dystrophy, and many studies have proposed mechanisms that bridge these two pathological conditions at the molecular level. In this review, the evidence indicating a causal role of oxidative stress in the pathogenesis of various muscular dystrophies is revisited. In particular, the mediation of cellular redox status in dystrophic muscle by NF-κB pathway, autophagy, telomere shortening, and epigenetic regulation are discussed. Lastly, the current stance of targeting these pathways using antioxidant therapies in preclinical and clinical trials is examined.
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spelling pubmed-47001982016-01-21 Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies Choi, Min Hee Ow, Jin Rong Yang, Nai-Di Taneja, Reshma Oxid Med Cell Longev Review Article Oxidative stress is a loss of balance between the production of reactive oxygen species during cellular metabolism and the mechanisms that clear these species to maintain cellular redox homeostasis. Increased oxidative stress has been associated with muscular dystrophy, and many studies have proposed mechanisms that bridge these two pathological conditions at the molecular level. In this review, the evidence indicating a causal role of oxidative stress in the pathogenesis of various muscular dystrophies is revisited. In particular, the mediation of cellular redox status in dystrophic muscle by NF-κB pathway, autophagy, telomere shortening, and epigenetic regulation are discussed. Lastly, the current stance of targeting these pathways using antioxidant therapies in preclinical and clinical trials is examined. Hindawi Publishing Corporation 2016 2015-12-22 /pmc/articles/PMC4700198/ /pubmed/26798425 http://dx.doi.org/10.1155/2016/6842568 Text en Copyright © 2016 Min Hee Choi et al. https://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
Choi, Min Hee
Ow, Jin Rong
Yang, Nai-Di
Taneja, Reshma
Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies
title Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies
title_full Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies
title_fullStr Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies
title_full_unstemmed Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies
title_short Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies
title_sort oxidative stress-mediated skeletal muscle degeneration: molecules, mechanisms, and therapies
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700198/
https://www.ncbi.nlm.nih.gov/pubmed/26798425
http://dx.doi.org/10.1155/2016/6842568
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