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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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.</description><identifier>ISSN: 1942-0900</identifier><identifier>ISSN: 1942-0994</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/5136957</identifier><identifier>PMID: 32566086</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>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</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-11, Article 5136957</ispartof><rights>Copyright © 2020 Wei-Xing Ma et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Wei-Xing Ma et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Wei-Xing Ma et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>31</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000540531700001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c565t-40d2db06c47613f39a6f50e40e95f3bc2e287f639867f39b84f8ff50cfb6f9ca3</citedby><cites>FETCH-LOGICAL-c565t-40d2db06c47613f39a6f50e40e95f3bc2e287f639867f39b84f8ff50cfb6f9ca3</cites><orcidid>0000-0003-4455-4980 ; 0000-0002-5815-5430 ; 0000-0002-4457-7376</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7277050/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7277050/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,4025,27928,27929,27930,28253,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32566086$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gomes, Aldrin V.</contributor><contributor>Aldrin V Gomes</contributor><creatorcontrib>Wang, Xin-Ping</creatorcontrib><creatorcontrib>Tao, Ran</creatorcontrib><creatorcontrib>Li, Chun-Yan</creatorcontrib><creatorcontrib>Ma, Wei-Xing</creatorcontrib><creatorcontrib>Yan, Liang-Jun</creatorcontrib><title>Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy</title><title>Oxidative medicine and cellular longevity</title><addtitle>OXID MED CELL LONGEV</addtitle><addtitle>Oxid Med Cell Longev</addtitle><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.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Cardiomyopathies - pathology</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Cardiomyopathy</subject><subject>Cell Biology</subject><subject>Deoxyribonucleic acid</subject><subject>Digital television</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Enzymes</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Kinases</subject><subject>Life Sciences & Biomedicine</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial DNA</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>Pathology</subject><subject>Prevention</subject><subject>Protein folding</subject><subject>Reactive Oxygen Species - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xin-Ping</au><au>Tao, Ran</au><au>Li, Chun-Yan</au><au>Ma, Wei-Xing</au><au>Yan, Liang-Jun</au><au>Gomes, Aldrin V.</au><au>Aldrin V Gomes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><stitle>OXID MED CELL LONGEV</stitle><addtitle>Oxid Med Cell Longev</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><artnum>5136957</artnum><issn>1942-0900</issn><issn>1942-0994</issn><eissn>1942-0994</eissn><abstract>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.</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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