Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

氧化应激 活性氧 细胞生物学 神经退行性变 信号转导 线粒体 生物 炎症 氧化磷酸化 生物化学 医学 免疫学 内科学 疾病
作者
Kai Wang,Yanhan Dong,Jing Liu,Lili Qian,Tao Wang,Xiangqian Gao,Kun Wang,Luqian Zhou
出处
期刊:Oxidative Medicine and Cellular Longevity [Hindawi Publishing Corporation]
卷期号:2020: 1-13 被引量:12
标识
DOI:10.1155/2020/5860356
摘要

Reduction oxidation (REDOX) reaction is crucial in life activities, and its dynamic balance is regulated by ROS. Reactive oxygen species (ROS) is associated with a variety of metabolic diseases involving in multiple cellular signalling in pathologic and physiological signal transduction. ROS are the by-products of numerous enzymatic reactions in various cell compartments, including the cytoplasm, cell membrane, endoplasmic reticulum (ER), mitochondria, and peroxisome. ROS signalling is not only involved in normal physiological processes but also causes metabolic dysfunction and maladaptive responses to inflammatory signals, which depends on the cell type or tissue environment. Excess oxidants are able to alter the normal structure and function of DNA, lipids, and proteins, leading to mutations or oxidative damage. Therefore, excessive oxidative stress is usually regarded as the cause of various pathological conditions, such as cancer, neurodegeneration, cardiovascular diseases (CVDs), diabetes, and kidney diseases. Currently, it has been possible to detect diabetes and other cardiac diseases by detecting derivatives accompanied by oxidative stress in vivo as biomarkers, but there is no effective method to treat these diseases. In consequence, it is essential for us to seek new therapy targeting these diseases through understanding the role of ROS signalling in regulating metabolic activity, inflammatory activation, and cardiac diseases related to metabolic dysfunction. In this review, we summarize the current literature on REDOX and its role in the regulation of cardiac metabolism and inflammation, focusing on ROS, local REDOX signalling pathways, and other mechanisms.

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