Sodium-glucose cotransporter 2 (SGLT2) inhibitors represent a novel class of therapeutic agents for treating diabetic kidney disease. These drugs primarily act by inhibiting the reabsorption of sodium and glucose in the renal proximal tubules, thereby exerting hypoglycemic effects. Emerging evidence indicates that SGLT2 inhibitors can effectively slow the progression of chronic kidney disease (CKD) and reduce cardiovascular risk in CKD patients with or without type 2 diabetes mellitus (T2DM). However, the mechanisms underlying their cardiorenal protective effects remain incompletely understood. Fibrosis in the heart and kidneys is a central pathological process driving CKD progression and cardiovascular dysfunction, and accumulating research suggests that SGLT2 inhibitors modulate cardiac and renal fibrosis. Despite these observations, the precise molecular and cellular pathways involved are not fully elucidated. This review aims to provide a comprehensive overview of the potential mechanisms through which SGLT2 inhibitors regulate cardiac and renal fibrosis.
Huang et al. (Thu,) studied this question.