TGF- β Study on the Role of Iron Death Signal Transduction in Diabetes Nephropathy

Abstract

DN (Diabetes Nephropathy) is the result of multiple factors, and its pathogenesis is complex. Extensive evidence has proven TGF- β. It plays an important role in the pathogenesis of DN, but the specific way of action is still unclear. TGF- β after binding and activating its receptor, its signal transmission needs to be carried out by a series of post receptor signal molecules TGF- β. It is the last and common important mediator of kidney damage caused by changes in biochemical factors and cytokines, such as blood glucose rise in diabetes. It can directly lead to DN characteristic pathological changes such as renal cell hypertrophy, excessive accumulation of extracellular matrix, glomerulosclerosis, renal interstitial fibrosis, etc. In DN, TGF- β the characteristic function of the β - lactamase is to stimulate the matrix deposition in the mesangial region. Through TGF- β. Further study on the role of DN iron death signal transduction in diabetes islets β the research on the mechanism of cell injury is reviewed. At the same time, it can not only increase the synthesis of extracellular matrix, but also inhibit the degradation of extracellular matrix components.