尿酸肾损伤的分子机制研究进展

Molecular mechanism of uric acid in renal injury

高尿酸血症(HUA)长期以来被认为是痛风的致病因子,但近年来大量的流行病学和临床研究表明高尿酸血症在肾损伤的发病和发展中起了重要作用。研究表明还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶、肾素—血管紧张素—醛固酮系统(RAAS)、丝裂原激活蛋白激酶(MAPK)信号、转化生长因子-β(TGF-β)、上皮间质转型等都单独的或共同的参与了肾病的发生和发展过程。目前研究争论的焦点主要集中在尿酸诱导肾损伤中的确切机制,该文主要根据现有的研究成果系统性地总结尿酸在肾损伤中的确切作用及可能的病理生理学分子机制。

Hyperuricemia has long been regarded as the major pathogenic factor in gout.A lot of epidemiological and clinical studies in recent years have accumulated that hyperuricemia may play an important role in the pathogenesis and progression of renal injury.Recent studies suggested nicotinamide adenine dinucleotide phosphate oxidase （NADPH oxidase）,the renin-angiotensin aldosterone system （RAAS）,mitogen-activatedproteinkinases （MAPK）signals,transforming growth factor β（TGF-β）,phenotypic transition of renal tubu-lar cells,etc.are activated during the course of renal injury and that these pathways individually or collectively play a role in the induc-tion and progression of renal injury.Now,controversy regarding the exact role of hyperuricemia in inducing the renal injury remains to be unfolded,the focus of this review is to systematically summarize the available evidence supporting the exact roles and mechanisms for u-ric acid in the development of renal injury and the potential pathophysiological molecular mechanisms involved.