Abstract:
The incidence of chronic kidney disease(CKD)has been rising yearly. And it has become one of the major hazards to public health in the world. The underlying causes of CKD include primary/secondary glomerulonephritis,diabetic nephropathy,hypertensive renal damage,renal tubulointerstitial lesions and genetic disorder,etc. Diabetic kidney disease(DKD),one of the causes of CKD,is a complication of diabetic renal microangiopathy and end-stage renal disease ensues if left unchecked. The specific pathogenesis of DKD has remained elusive. Hyperglycemia causes immune-mediated inflammation and renal injuries. However,immune-mediated inflammatory factors are one of the important causes of DKD. During hyperglycemia,such inflammatory response cells as interleukin and tumor necrosis factors are mobilized to infiltrate kidney and stimulate the development of renal microangiopathy through a large variety of signaling pathways. In recent years,Toll-like receptor 4(TLR4)and NoD-like receptor family pyrin domain-containing protein 3(NLRP3)play an important role in renal-related immune inflammatory diseases. And TLR4/NLRP3 inflammatory bodies are closely correlated with the pathogenesis of DKD. Elevated TLR4 level has been detected under hyperglycemia. However,TLR4 stimulates the maturation and release of downstream inflammatory factors by activating NF-κB through recognizing specific ligands and NLRP3 inflammatory bodies exist sparsely in mesangial cells of DKD. The activation of NF-κB activates the assembly and maturation of inflammatory bodies,thus promoting the release of inflammatory cytokines. Thus TLR4 and NLRP3 play some important roles in the development of diabetic nephropathy.