Key result
SGLT2i and GLP-1RA protect against diabetic cardiomyopathy by mitigating fibrosis and improving mitochondrial function.
Why the study?
The molecular mechanisms underlying diabetic cardiomyopathy are not yet fully understood, early stages are often asymptomatic, and distinct biomarkers are lacking.
Understanding the molecular pathways of diabetic cardiomyopathy provides a rationale for using specific anti-hyperglycemic drugs like SGLT2 inhibitors to prevent or delay early myocardial injury.
Answers are grounded in this paper and cite their sources.
Supports mechanistic rationale for SGLT2 inhibitors and GLP-1 receptor agonists in diabetic cardiomyopathy; leaves open confirmation in prospective outcome trials.
Epidemiological evidence has shown that diabetes is associated with overt heart failure (HF) and worse clinical outcomes. However, the presence of a distinct primary diabetic cardiomyopathy (DCM) has not been easy to prove because the association between diabetes and HF is confounded by hypertension, obesity, microvascular dysfunction, and autonomic neuropathy. In addition, the molecular mechanisms underlying DCM are not yet fully understood, DCM usually remains asymptomatic in the early stage, and no specific biomarkers have been identified. Nonetheless, several mechanistic associations at the systemic, cardiac, and cellular/molecular levels explain different aspects of myocardial dysfunction, including impaired cardiac relaxation, compliance, and contractility. In this review, we focus on recent clinical and preclinical advances in our understanding of the molecular mechanisms of DCM and the role of anti-hyperglycemic agents in preventing DCM beyond their glucose lowering effect.
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Lee et al. (2025) conducted a review in Diabetic cardiomyopathy. Anti-hyperglycemic drugs was evaluated. SGLT2 inhibitors and GLP-1 receptor agonists exhibit cardioprotective effects in diabetic cardiomyopathy beyond glucose lowering by mitigating fibrosis and improving mitochondrial function.
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