Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center (UNTHSC), Fort Worth, Texas 76107, USA.
Qingdao University of Science and Technology, 266042 Qingdao, Shandong, China.
Oxid Med Cell Longev. 2020 May 29;2020:5136957. doi: 10.1155/2020/5136957. eCollection 2020.
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.
本综述的目的是总结过去五年中关于细胞还原性应激诱导的线粒体功能障碍、二硫苏糖醇（DTT）诱导的还原性应激和还原性应激相关自由基反应的研究报告。还原性应激在抗氧化和疾病诱导方面被认为是一把双刃剑。由于许多潜在的机制尚不清楚，显然需要进一步的研究。然而，还原性应激被认为是由细胞还原能力的升高引起的，如 NADH、谷胱甘肽和 NADPH；最近，这一研究领域引起了越来越多的关注。尽管如此，我们认为有必要进一步研究，以确定更多的指标来评估和预防心脏损伤的风险，并探索更多的治疗心肌病的靶点。因此，预计还原性应激诱导的线粒体功能障碍的潜在机制的进一步研究将为改善还原性应激诱导的心肌病的治疗方法提供新的见解。
