Myocardial Fibrosis in Diabetic Cardiomyopathy: Mechanisms, Implications, and Therapeutic Perspectives.

Abstract

Diabetic cardiomyopathy (DCM) represents a distinct form of heart disease characterized by structural and functional alterations in the myocardium, occurring in the absence of other cardiac conditions. This review delves into the pathophysiological mechanisms underlying myocardial fibrosis in DCM, highlighting the pivotal role of fibroblast transdifferentiation into myofibroblasts. We examine the interplay between hyperglycemia, immune cell activation, and neurohumoral signaling pathways, with a particular focus on the transforming growth factor-beta (TGF-β) signaling cascade and its contributions to collagen deposition and cardiac dysfunction. Despite significant advancements in understanding the cellular and molecular mechanisms of DCM, critical gaps remain in elucidating the precise regulatory networks involved in fibroblast activation and the role of microRNAs in these processes. By providing a comprehensive overview of current knowledge, this review aims to identify potential therapeutic targets to mitigate myocardial fibrosis and improve clinical outcomes in diabetic patients. Ultimately, addressing these gaps will pave the way for novel therapeutic strategies that can enhance heart function and reduce the burden of diabetic cardiomyopathy.