摘要
尿酸是人体嘌呤代谢的最终产物.当尿酸生成过多或排泄减少时,尿酸在体内过度积累可导致高尿酸血症.高尿酸血症被认为是肾脏损伤和慢性肾脏病的独立危险因素.当尿酸浓度超过正常生理范围时可引起肾小管的多种病理反应,但其病理生理机制尚不完全清楚.本文就高尿酸血症导致肾小管损伤的分子机制进行综述,包括高尿酸血症中尿酸诱导的自噬、炎症、氧化应激、凋亡、上皮-间充质转化和纤维化等过程.
Abstract
Uric acid is the final product of purine metabolism in the human body.When uric acid is produced too much or excreted is reduced,excessive accumulation of uric acid in the body can lead to hyperuricemia.Hyperuricemia is considered to be an independent risk factor for kidney damage and chronic kidney disease.When the concentration of uric acid exceeds the normal physiological range,it can cause a variety of pathological reactions in the renal tubules,but its pathophysiological mechanism is not fully understood.This article reviews the molecular mechanisms of renal tubular damage caused by hyperuricemia,including autophagy,inflammation,oxidative stress,apoptosis,epithelial-mesenchymal transition,fibrosis,and other processes induced by uric acid in hyperuricemia.
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