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尿酸在炎症和动脉粥样硬化发病机制中的作用。

Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis.

机构信息

Department of Internal Medicine, Faculty of Medicine, Teikyo University of Medicine, Tokyo 173-8605, Japan.

Department of Microbiology and Immunology, Faculty of Medicine, Teikyo University of Medicine, Tokyo 173-8605, Japan.

出版信息

Int J Mol Sci. 2021 Nov 17;22(22):12394. doi: 10.3390/ijms222212394.

Abstract

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.

摘要

高尿酸血症是一种常见的代谢综合征。尿酸水平升高是痛风、高血压和慢性肾脏病的危险因素。此外,各种流行病学研究也表明心血管风险与高尿酸血症之间存在关联。在高尿酸血症中,黄嘌呤氧化酶同时形成尿酸时会产生活性氧 (ROS)。细胞内尿酸也被报道会促进 ROS 的产生。ROS 和细胞内尿酸本身调节几种细胞内信号通路,这些通路的改变可能导致动脉粥样硬化病变的发展。在这篇综述中,我们描述了尿酸对各种分子信号的影响以及高尿酸血症中动脉粥样硬化发展的潜在机制。此外,我们还讨论了高尿酸血症治疗的疗效,以防止动脉粥样硬化的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7948/8624633/739452637db7/ijms-22-12394-g001.jpg

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