高尿酸血症
尿酸
痛风
发病机制
细胞内
炎症
活性氧
黄嘌呤氧化酶
医学
氧化应激
内科学
内分泌学
生物化学
化学
生物
酶
作者
Yoshitaka Kimura,Daisuke Tsukui,Hajime Kono
标识
DOI:10.3390/ijms222212394
摘要
Hyperuricemia is a common metabolic syndrome. Elevated uric acid levels are risk factors for gout, hypertension, and chronic kidney diseases. Furthermore, various epidemiological studies have also demonstrated an association between cardiovascular risks and hyperuricemia. In hyperuricemia, reactive oxygen species (ROS) are produced simultaneously with the formation of uric acid by xanthine oxidases. Intracellular uric acid has also been reported to promote the production of ROS. The ROS and the intracellular uric acid itself regulate several intracellular signaling pathways, and alterations in these pathways may result in the development of atherosclerotic lesions. In this review, we describe the effect of uric acid on various molecular signals and the potential mechanisms of atherosclerosis development in hyperuricemia. Furthermore, we discuss the efficacy of treatments for hyperuricemia to protect against the development of atherosclerosis.
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