Mechanisms of Inflammation-Fibrosis in Diabetic Nephropathy and Intervention Strategies of Traditional Chinese and Western Medicine

Abstract

Diabetic nephropathy (DKD) is one of the most serious microvascular complications of diabetes. Its pathological process has expanded from a simple metabolic disorder to an "inflammation-fibrosis continuum." Under conditions of high glucose, oxidative stress, and lipotoxicity, immune cell infiltration and abnormal activation of signaling pathways such as NF-κB, NLRP3 inflammasome, and JAK/STAT drive persistent inflammatory responses. Subsequently, fibrosis-related pathways such as TGFβ/Smad and Wnt/β-catenin are significantly upregulated, leading to excessive extracellular matrix deposition, epithelial-mesenchymal transition, and fibroblast activation, ultimately resulting in irreversible renal fibrosis. In terms of treatment, Western medicine drugs such as ACEIs/ARBs, SGLT2 inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and GLP-1 receptor agonists have shown new advantages in delaying disease progression and inhibiting inflammatory fibrosis. Traditional Chinese medicine, through multi-component and multi-target effects, inhibits key pathways such as NF-κB and TGFβ/Smad, improving the progression of inflammation and fibrosis. Clinical and experimental studies suggest that the integration of traditional Chinese medicine (TCM) and Western medicine can create a synergistic effect in controlling metabolism, reducing inflammation, and combating fibrosis, significantly improving proteinuria and renal function. In the future, with the application of biomarkers, in-depth research into molecular mechanisms, and the promotion of the integrated TCM and Western medicine model, the prevention and treatment of diabetic kidney disease (DKD) is expected to enter a new, more precise and comprehensive stage.