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尿酸在心房颤动发病机制中的氧化应激、炎症、纤维化、细胞凋亡及免疫过程中的关键作用

The Key Role of Uric Acid in Oxidative Stress, Inflammation, Fibrosis, Apoptosis, and Immunity in the Pathogenesis of Atrial Fibrillation.

作者信息

Deng Yawen, Liu Fei, Yang Xiaolei, Xia Yunlong

机构信息

Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, China.

出版信息

Front Cardiovasc Med. 2021 Feb 26;8:641136. doi: 10.3389/fcvm.2021.641136. eCollection 2021.

Abstract

Atrial fibrillation (AF) is a highly prevalent cardiac arrhythmia that leads to numerous adverse outcomes including stroke, heart failure, and death. Hyperuricemia is an important risk factor that contributes to atrium injury and AF, but the underlying molecular mechanism remains to be elucidated. In this review, we discussed the scientific evidence for clarifying the role of hyperuricemia in the pathogenesis of AF. Experimental and Clinical evidence endorse hyperuricemia as an independent risk factor for the incidence of AF. Various and investigations showed that hyperuricemia might play a critical role in the pathogenesis of AF at different UA concentrations through the activation of oxidative stress, inflammation, fibrosis, apoptosis, and immunity.

摘要

心房颤动(AF)是一种高度常见的心律失常,可导致包括中风、心力衰竭和死亡在内的多种不良后果。高尿酸血症是导致心房损伤和房颤的重要危险因素,但其潜在的分子机制仍有待阐明。在本综述中,我们讨论了阐明高尿酸血症在房颤发病机制中作用的科学证据。实验和临床证据支持高尿酸血症是房颤发生的独立危险因素。各种研究表明,高尿酸血症可能通过激活氧化应激、炎症、纤维化、细胞凋亡和免疫反应,在不同尿酸浓度下在房颤的发病机制中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6a0/7952317/d2250aa47bfc/fcvm-08-641136-g0001.jpg

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