Department of Physiology, College of Medicine, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Reproductive Biology and Toxicology Research Laboratories, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria.
Lipids Health Dis. 2021 Feb 27;20(1):23. doi: 10.1186/s12944-021-01435-7.
Oxidative stress, an alteration in the balance between reactive oxygen species (ROS) generation and antioxidant buffering capacity, has been implicated in the pathogenesis of cardiometabolic disorders (CMD). At physiological levels, ROS functions as signalling mediators, regulates various physiological functions such as the growth, proliferation, and migration endothelial cells (EC) and smooth muscle cells (SMC); formation and development of new blood vessels; EC and SMC regulated death; vascular tone; host defence; and genomic stability. However, at excessive levels, it causes a deviation in the redox state, mediates the development of CMD. Multiple mechanisms account for the rise in the production of free radicals in the heart. These include mitochondrial dysfunction and uncoupling, increased fatty acid oxidation, exaggerated activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX), reduced antioxidant capacity, and cardiac metabolic memory. The purpose of this study is to discuss the link between oxidative stress and the aetiopathogenesis of CMD and highlight associated mechanisms. Oxidative stress plays a vital role in the development of obesity and dyslipidaemia, insulin resistance and diabetes, hypertension via various mechanisms associated with ROS-led inflammatory response and endothelial dysfunction.
氧化应激是活性氧（ROS）生成和抗氧化缓冲能力之间平衡的改变，与心脏代谢紊乱（CMD）的发病机制有关。在生理水平上，ROS 作为信号介质发挥作用，调节各种生理功能，如内皮细胞（EC）和平滑肌细胞（SMC）的生长、增殖和迁移；新血管的形成和发育；EC 和 SMC 调节死亡；血管张力；宿主防御；和基因组稳定性。然而，在过量水平下，它会导致氧化还原状态的偏离，介导 CMD 的发展。多种机制导致心脏自由基产生增加。这些机制包括线粒体功能障碍和解偶联、脂肪酸氧化增加、烟酰胺腺嘌呤二核苷酸磷酸氧化酶（NOX）活性过度、抗氧化能力降低和心脏代谢记忆。本研究的目的是讨论氧化应激与 CMD 的发病机制之间的联系，并强调相关机制。氧化应激通过与 ROS 介导的炎症反应和内皮功能障碍相关的各种机制，在肥胖和血脂异常、胰岛素抵抗和糖尿病、高血压的发展中起着至关重要的作用。
