高尿酸血症
痛风
尿酸
医学
发病机制
生物信息学
炎症
内科学
生物
作者
Michael H. Pillinger,Pamela Rosenthal,Aryeh M. Abeles
出处
期刊:Bulletin of the NYU hospital for joint diseases
日期:2007-09-01
卷期号:65 (3): 215-215
被引量:14
摘要
Over the past decade, significant advances have been made regarding the pathogenesis, clinical implications, and treatment of hyperuricemia. While physicians have understood for at least a century that uric acid causes gout, we are now beginning to address the question of why hyperuricemia exists and the mechanisms by which uric acid acts to stimulate inflammation. This review focuses on (1) previously unknown biological roles of uric acid; (2) why the loss of the uricase gene and resultant hyperuricemia may have provided an evolutionary advantage to primates and, in particular, to humans; (3) the molecular effects of uric acid on inflammatory cells; and (4) novel antihyperuricemic agents currently under study.
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