Why the study?
Patients with diabetes have an increased risk of heart failure from diabetic cardiomyopathy, driving interest in exploring the underlying molecular mechanisms to identify new therapeutic strategies.
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Design
Review
Hypothesis-generating on DCM pathways in diabetes; leaves open whether targeting them alters HF risk.
Cardiovascular complications, particularly diabetic cardiomyopathy (DCM), are the primary causes of morbidity and mortality among individuals with diabetes. Hyperglycemia associated with diabetes leads to cardiomyocyte hypertrophy, apoptosis, and myocardial fibrosis, culminating in heart failure (HF). Patients with diabetes face a 2-4 times greater risk of developing HF compared with those without diabetes. Consequently, there is a growing interest in exploring the molecular mechanisms that contribute to the development of DCM. MicroRNAs (miRNAs) are short, single-stranded, noncoding RNA molecules that participate in the maintenance of physiological homeostasis through the regulation of essential processes such as metabolism, cell proliferation, and apoptosis. At the posttranscriptional level, miRNAs modulate gene expression by binding directly to genes' mRNAs. Multiple cardiac-enriched miRNAs were reported to be dysregulated under diabetic conditions. Different studies revealed the role of specific miRNAs in the pathogenesis of diabetes and related cardiovascular complications, including cardiomyocyte hypertrophy and fibrosis, mitochondrial dysfunction, metabolic impairment, inflammatory response, or cardiomyocyte death. Circulating miRNAs have been shown to represent the potential biomarkers for early detection of diabetic heart injury. A deeper understanding of miRNAs and their role in diabetes-related pathophysiological processes could lead to new therapeutic strategies for addressing cardiac complications associated with diabetes.
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Kura et al. (2025) studied this question.
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