Key result
Diabetic cardiomyopathy progression stems from cell death, exosome dysregulation, fibrosis, and epicardial adipose inflammation.
This review consolidates the complex molecular and cellular mechanisms underlying diabetic cardiomyopathy to highlight potential future therapeutic targets.
May guide multi-pathway therapeutic exploration in diabetic cardiomyopathy; leaves open prioritization of targets for prospective trials.
Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left ventricular hypertrophy and diastolic dysfunction, and the second by heart failure (HF) with systolic dysfunction. The proposed mechanisms involve cardiac inflammation, advanced glycation end products (AGEs) and angiotensin II. Furthermore, different studies have focused their attention on cardiomyocyte death through the different mechanisms of programmed cell death, such as apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. Exosome release, adipose epicardial tissue and aquaporins affect DCM development. This review will focus on the description of the mechanisms involved in DCM progression and development.
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Galeone et al. (2024) conducted a review in Diabetic Cardiomyopathy. Diabetic cardiomyopathy progression is driven by multiple mechanisms including programmed cell death, exosome dysregulation, cardiac fibrosis, and epicardial adipose tissue inflammation.
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