Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies.

Diabetic cardiomyopathy (DCM) is a common complication of diabetes, characterized by myocardial injury, fibrosis, and heart dysfunction. The pathogenesis remains poorly understood, with limited treatment options. Recent research highlights the roles of regulated cell death (RCD) and inflammation in DCM progression. RCD types, including apoptosis, pyroptosis, ferroptosis, and necroptosis, are central to myocardial damage and are closely linked to oxidative stress and inflammation. Inflammatory pathways like NLRP3, NF-κB, and TLR4 activate cytokines (TNF-α, IL-1β, IL-6), exacerbating fibrosis and heart failure. Notably, RCD and inflammation create a feedback loop, amplifying each other and accelerating DCM. This review explores the interactions between RCD and inflammatory signaling, their contribution to myocardial injury, and potential therapeutic strategies targeting both pathways. A multi-targeted approach to DCM therapy may offer new avenues for treatment.