Browsing by Subject "Oxidation-Reduction"
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Item Involvement of Nrf2 in Ocular Diseases(Hindawi, 2017-03-27) Batliwala, Shehzad; Xavier, Christy; Liu, Yang; Wu, Hongli; Pang, Iok-HouThe human body harbors within it an intricate and delicate balance between oxidants and antioxidants. Any disruption in this checks-and-balances system can lead to harmful consequences in various organs and tissues, such as the eye. This review focuses on the effects of oxidative stress and the role of a particular antioxidant system-the Keap1-Nrf2-ARE pathway-on ocular diseases, specifically age-related macular degeneration, cataracts, diabetic retinopathy, and glaucoma. Together, they are the major causes of blindness in the world.Item Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease(MDPI, 2022-03-21) Yan, Liang-JunNote: In lieu of an abstract, this is an excerpt from the first page. The kidneys carry out fundamental life-sustaining functions by removing waste substances, controlling salt and water balance, retaining substances vital to the body such as glucose and proteins, and maintaining blood pH balance.Item Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy(Hindawi, 2020-05-29) Ma, Wei-Xing; Li, Chun-Yan; Tao, Ran; Wang, Xin-Ping; Yan, Liang-JunThe 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.