Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy

The goal of this review was to summarize reported studies focusing on cellular reductive stress-induced mitochondrial dysfunction, cardiomyopathy, dithiothreitol- (DTT-) induced reductive stress, and reductive stress-related free radical reactions published in the past five years. Reductive stress i...

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Veröffentlicht in:Oxidative medicine and cellular longevity 2020, Vol.2020 (2020), p.1-11, Article 5136957
Hauptverfasser: Wang, Xin-Ping, Tao, Ran, Li, Chun-Yan, Ma, Wei-Xing, Yan, Liang-Jun
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container_issue 2020
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container_title Oxidative medicine and cellular longevity
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creator Wang, Xin-Ping
Tao, Ran
Li, Chun-Yan
Ma, Wei-Xing
Yan, Liang-Jun
description The goal of this review was to summarize reported studies focusing on cellular reductive stress-induced mitochondrial dysfunction, cardiomyopathy, dithiothreitol- (DTT-) induced reductive stress, and reductive stress-related free radical reactions published in the past five years. Reductive stress is considered to be a double-edged sword in terms of antioxidation and disease induction. As many underlying mechanisms are still unclear, further investigations are obviously warranted. Nonetheless, reductive stress is thought to be caused by elevated levels of cellular reducing power such as NADH, glutathione, and NADPH; and this area of research has attracted increasing attention lately. Albeit, we think there is a need to conduct further studies in identifying more indicators of the risk assessment and prevention of developing heart damage as well as exploring more targets for cardiomyopathy treatment. Hence, it is expected that further investigation of underlying mechanisms of reductive stress-induced mitochondrial dysfunction will provide novel insights into therapeutic approaches for ameliorating reductive stress-induced cardiomyopathy.
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Reductive stress is considered to be a double-edged sword in terms of antioxidation and disease induction. As many underlying mechanisms are still unclear, further investigations are obviously warranted. Nonetheless, reductive stress is thought to be caused by elevated levels of cellular reducing power such as NADH, glutathione, and NADPH; and this area of research has attracted increasing attention lately. Albeit, we think there is a need to conduct further studies in identifying more indicators of the risk assessment and prevention of developing heart damage as well as exploring more targets for cardiomyopathy treatment. Hence, it is expected that further investigation of underlying mechanisms of reductive stress-induced mitochondrial dysfunction will provide novel insights into therapeutic approaches for ameliorating reductive stress-induced cardiomyopathy.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32566086</pmid><doi>10.1155/2020/5136957</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-4455-4980</orcidid><orcidid>https://orcid.org/0000-0002-5815-5430</orcidid><orcidid>https://orcid.org/0000-0002-4457-7376</orcidid><oa>free_for_read</oa></addata></record>
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subjects Animals
Antioxidants
Cardiomyopathies - pathology
Cardiomyopathies - physiopathology
Cardiomyopathy
Cell Biology
Deoxyribonucleic acid
Digital television
DNA
DNA damage
Enzymes
Heart diseases
Humans
Hypoxia
Kinases
Life Sciences & Biomedicine
Metabolism
Mitochondria
Mitochondria - pathology
Mitochondrial DNA
Oxidation
Oxidation-Reduction
Oxidative Stress
Pathology
Prevention
Protein folding
Reactive Oxygen Species - metabolism
Review
Science & Technology
Signal Transduction
title Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy
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