Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy

被引:37
|
作者
Ma, Wei-Xing [1 ,2 ]
Li, Chun-Yan [1 ,3 ]
Tao, Ran [4 ]
Wang, Xin-Ping [2 ]
Yan, Liang-Jun [1 ]
机构
[1] Univ North Texas Hlth Sci Ctr UNTHSC, UNT Syst Coll Pharm, Dept Pharmaceut Sci, Ft Worth, TX 76107 USA
[2] Qingdao Univ Sci & Technol, Qingdao 266042, Shandong, Peoples R China
[3] Shantou Univ, Med Coll, Shantou 515041, Guangdong, Peoples R China
[4] Qingdao Municipal Ctr Dis Control & Prevent, Qingdao 266034, Shandong, Peoples R China
关键词
ALPHA-B-CRYSTALLIN; SHOCK-PROTEIN; 27; OXIDATIVE STRESS; REDOX IMBALANCE; VASCULAR DYSFUNCTION; DNA-DAMAGE; HEART; DITHIOTHREITOL; GLUTATHIONE; AUTOPHAGY;
D O I
10.1155/2020/5136957
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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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收藏
页数:11
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