Diabetic nephropathy has a prevalence of 20%-40% in diabetic patients and is one of the most important causes of end-stage renal disease, and the prevention and treatment of diabetic nephropathy is gradually receiving widespread attention worldwide. The development of diabetic nephropathy may be related to genetic susceptibility, disorders of glucose and lipid metabolism and altered glomerular hemodynamics. The cytokine network is an important target for prevention and treatment. It is a core factor in the complex cytokine network of diabetic nephropathy and is involved in the regulation of many cellular functions. In addition to mediating the pathological effects of hyperglycemia, it also mediates the pathophysiological changes of hemodynamic, non-enzymatic glycosylation, angiotensin and endothelin pathways. MAPKs, ERK and P38, which ultimately lead to extracellular matrix accumulation and renal fibrosis. Basic research has shown that reducing TGF-β activity can slow down the progression of diabetic nephropathy. Currently, the methods available to specifically block the TGF-β system include TGF-β neutralizing antibodies, TGF-β receptor kinase blockers, Smad7 overexpression, antisense oligonucleotide technology and small interfering RNA technology. 2. Foot cells In 2000, Ziyaden et al. found that blocking the TGF-β/Smad signaling system could not improve proteinuria caused by diabetic nephropathy in db/db mice. Recent studies have shown that proteinuria in diabetic nephropathy is closely related to glomerular podocyte injury and the role of podocyte-derived vascular endothelial growth factor (VEGF). VEGF expression is upregulated in diabetic nephropathy, and VEGF may act on podocytes in an autocrine manner and glomerular endothelial cells in a paracrine manner, increasing glomerular endothelial cell permeability and causing blood rheological changes by stimulating nitric oxide, and also changing the structure of the glomerular basement membrane filtration barrier to cause proteinuria. It was found that SU5416, a VEGF receptor agonist blocker, was effective in treating proteinuria and improving renal tissue damage in db/db mice. Therefore, the role of podocytes in the mechanism of proteinuria in diabetic nephropathy has been emphasized, and the role of podocyte-derived VEGF is particularly important. Although there is more evidence that ACEI and ARB can improve proteinuria and protect renal function in patients with diabetic nephropathy, long-term follow-up results indicate that the progression of renal lesions continues. In view of the involvement of many factors in the pathogenesis of diabetic nephropathy, new ideas advocate the use of multiple drugs in combination to block the progression of diabetic nephropathy through different pathways. Some of the new therapies being investigated are: sulodexide, endothelin receptors, pyridoxamine, PKC-b, cyclooxygenase 2, Aldo/Eplenerone, Pirfenidone and relaxin. It is hoped that the progression of diabetic nephropathy can be effectively reversed and stopped by multi-path therapy.