Biomedical Research Center, College of Medicine, and Department of Biomedical Sciences, College of Health Sciences, Qatar University, P.O. Box 2713, Doha, Qatar.
Faculty of Medicine, American University of Beirut, 11-0236 Beirut, Lebanon.
Front Biosci (Landmark Ed). 2022 Mar 18;27(3):105. doi: 10.31083/j.fbl2703105.
Cardiovascular disease (CVD) is a major cause of mortality worldwide. A better understanding of the mechanisms underlying CVD is key for better management or prevention. Oxidative stress has been strongly implicated in the pathogenesis of CVD. Indeed, several studies demonstrated that reactive oxygen species (ROS), via different mechanisms, can lead to endothelial cell (EC) dysfunction, a major player in the etiology of several CVDs. ROS appears to modulate a plethora of EC biological processes that are critical for the integrity of the endothelial function. This review seeks to dissect the role of oxidative stress-induced endothelial dysfunction in CVD development, with emphasis on the underlying mechanisms and pathways. Special attention is given to ROS-induced reduction of NO bioavailability, ROS-induced inflammation, and ROS-induced mitochondrial dysfunction. A better understanding and appraisal of these pathways may be essential to attenuate oxidative stress or reverse EC dysfunction, and hence, reduce CVD burden.
心血管疾病（CVD）是全球范围内主要的死亡原因。更好地理解 CVD 发病机制对于更好地管理或预防至关重要。氧化应激强烈参与 CVD 的发病机制。事实上，几项研究表明，活性氧（ROS）通过不同的机制可导致内皮细胞（EC）功能障碍，这是多种 CVD 的主要病因之一。ROS 似乎调节了许多对内皮功能完整性至关重要的 EC 生物学过程。本综述旨在剖析氧化应激诱导的内皮功能障碍在 CVD 发展中的作用，重点关注潜在的机制和途径。特别关注 ROS 诱导的 NO 生物利用度降低、ROS 诱导的炎症和 ROS 诱导的线粒体功能障碍。更好地理解和评估这些途径可能对于减轻氧化应激或逆转 EC 功能障碍从而降低 CVD 负担至关重要。
