摘要
糖尿病的 nephropathy (DN ) 是结束阶段的最普通的原因肾的疾病(ESRD ) 。关于有类型 1 和类型 2 糖尿病的人的 20%30% 开发 DN。DN 被 glomerulosclerosis 与 glomerular 地下室膜和 mesangial 矩阵变厚描绘扩大，和 tubulointerstitial 纤维变性。多糖症和在糖尿病的 intra 肾的高血压蛋白原酶血管收缩素系统(地岬) 的激活被建议了在 DN 的致病起一个关键作用。然而，机制不是众所周知的。
Diabetic nephropathy （DN） is the most common cause of end-stage renal disease （ESRD）. About 20%-30% of people with type 1 and type 2 diabetes develop DN. DN is characterized by both glomerulosclerosis with thickening of the glomerular basement membrane and mesangial matrix expansion, and tubulointerstitial fibrosis. Hyperglycemia and the activation of the intra-renal renin-angiotensin system （RAS） in diabetes have been suggested to play a critical role in the pathogenesis of DN. However, the mechanisms are not well known. Studies from our laboratory demonstrated that the transcription factor--upstream stimulatory factor 2 （USF2） is an important regulator of DN. Moreover, the renin gene is a downstream target of USF2. Importantly, USF2 transgenic （Tg） mice demonstrate a specific increase in renal renin expression and angiotensin II （AngII） levels in kidney and exhibit increased urinary albumin excretion and extracellular matrix deposition in glomeruli, supporting a role for USF2 in the development of diabetic nephropathy. In this review, we summarize our findings of the mechanisms by which diabetes regulates USF2 in kidney cells and its role in regulation of renal renin-angiotensin system and the development of diabetic nephropathy.
