Role of PPARγ, IL-1β Blockers, and TGF-β1 in Diabetic Wound Healing: Mechanisms and Therapeutic Potential

Diabetic foot ulcers are a major diabetes complication, particularly in regions with high prevalence and limited access to advanced care. Impaired healing in diabetic foot ulcers results from chronic inflammation, poor angiogenesis, extracellular matrix dysfunction, and metabolic imbalances. This review examines the roles of peroxisome proliferator-activated receptor gamma (PPARγ), interleukin-1 beta (IL-1β) blockers, and transforming growth factor beta 1 (TGF-β1) in diabetic wound healing. PPARγ suppresses inflammation and promotes tissue repair, but its function is often impaired in diabetes. IL-1β sustains inflammation and delays macrophage transition from M1 to M2, while TGF-β1 dysregulation disrupts collagen synthesis and extracellular matrix remodeling, contributing to fibrosis or delayed healing. These pathways are also implicated in diabetic retinopathy, where chronic inflammation and impaired angiogenesis worsen tissue damage. PPARγ agonists (e.g., rosiglitazone), IL-1β blockers (e.g., anakinra, canakinumab), and TGF-β1 modulators offer promising therapeutic strategies. While preclinical studies show potential, further clinical research is needed to refine treatment approaches and improve patient outcomes.