关键词: Endothelial dysfunctions ROS inflammation vascular cells. vascular physiology xanthine oxidoreductase

Mesh : Humans Xanthine Dehydrogenase / metabolism Endothelium, Vascular / physiopathology metabolism enzymology Reactive Oxygen Species / metabolism Oxidative Stress Animals Hypertension / physiopathology enzymology metabolism Cardiovascular Diseases / physiopathology enzymology metabolism Uric Acid / metabolism blood Enzyme Inhibitors / pharmacology

来  源:   DOI:10.2174/0115734021277772240124075120

Abstract:
Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in the formation of uric acid (UA) and is involved in the generation of reactive oxygen species (ROS). Overproduction of ROS has been linked to the pathogenesis of hypertension, atherosclerosis, and cardiovascular disease, with multiple studies over the last 30 years demonstrating that XOR inhibition is beneficial. The involvement of XOR and its constituents in the advancement of chronic inflammation and ROS, which are responsible for endothelial dysfunction, is the focus of this evidence-based review. An overabundance of XOR products and ROS appears to drive the inflammatory response, resulting in significant endothelium damage. It has also been demonstrated that XOR activity and ED are connected. Diabetes, hypertension, and cardiovascular disease are all associated with endothelial dysfunction. ROS mainly modifies the activity of vascular cells and can be important in normal vascular physiology as well as the development of vascular disease. Suppressing XOR activity appears to decrease endothelial dysfunction, probably because it lessens the generation of reactive oxygen species and the oxidative stress brought on by XOR. Although there has long been a link between higher vascular XOR activity and worse clinical outcomes, new research suggests a different picture in which positive results are mediated by XOR enzymatic activity. Here in this study, we aimed to review the association between XOR and vascular endothelial dysfunction. The prevention and treatment approaches against vascular endothelial dysfunction in atherosclerotic disease.
摘要:
黄嘌呤氧化还原酶(XOR)是尿酸(UA)形成中的限速酶,并参与活性氧(ROS)的产生。ROS的过量产生与高血压的发病机制有关,动脉粥样硬化,和心血管疾病,过去30年的多项研究表明,XOR抑制是有益的。XOR及其成分参与慢性炎症和ROS的进展,负责内皮功能障碍,是这次循证审查的重点。过量的XOR产品和ROS似乎驱动炎症反应,导致显著的内皮损伤。也已经证明XOR活性和ED是连接的。糖尿病,高血压,和心血管疾病都与内皮功能障碍有关。ROS主要修饰血管细胞的活性,在正常的血管生理以及血管疾病的发展中可能是重要的。抑制XOR活性似乎减少内皮功能障碍,可能是因为它减少了活性氧的产生和XOR带来的氧化应激。尽管血管XOR活性较高与临床结果较差之间存在长期联系,新的研究表明了一种不同的情况,其中阳性结果是由XOR酶活性介导的。在这项研究中,我们旨在综述XOR与血管内皮功能障碍之间的关系.动脉粥样硬化疾病中血管内皮功能障碍的预防和治疗方法。
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