Mechanisms of diabetic cardiomyopathy: Focus on inflammation

Abstract Purpose of Review Type 2 diabetes (T2D) significantly increases the risk of heart failure (HF), either through the progression of coronary artery disease (CAD) or through direct myocardial alterations, termed diabetic cardiomyopathy. This review examines key pathophysiological mechanisms underlying diabetic cardiomyopathy, focusing on the role of inflammation. It also addresses diagnostic and therapeutic approaches to mitigate myocardial damage in T2D. Recent Findings Chronic low‐grade inflammation is considered as a major contributor to diabetic cardiomyopathy. T2D‐related factors, including hyperglycemia and insulin resistance, activate inflammatory pathways that worsen myocardial dysfunction. Despite advances in understanding these mechanisms, no therapies specifically targeting the cardiac changes in T2D have been identified. Summary While significant advances have been made in elucidating the inflammatory mechanisms contributing to diabetic cardiomyopathy, therapeutic advancements remain limited, potentially due to an incomplete understanding of regulatory pathways. A comprehensive investigation into the specific roles of immune cells and inflammatory mediators in diabetic cardiomyopathy is essential for identifying novel therapeutic targets. Expanding our knowledge of these molecular mechanisms has the potential to facilitate the development of innovative therapeutic strategies, thereby improving clinical outcomes in patients with T2D.