Why the study?
Molecular pathomechanisms of diabetic cardiomyopathy remain incompletely understood, and no causative treatment exists to modulate or reverse cardiac dysfunction in diabetic patients.
This review summarizes current knowledge on the molecular mechanisms of diabetic cardiomyopathy and the utility of various animal models in understanding its pathogenesis.
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No causative therapy for diabetic cardiomyopathy; leaves open translation of animal mechanisms to human disease.
Diabetes mellitus increases the risk of heart failure independent of co-existing hypertension and coronary artery disease. Although several molecular mechanisms for the development of diabetic cardiomyopathy have been identified, they are incompletely understood. The pathomechanisms are multifactorial and as a consequence, no causative treatment exists at this time to modulate or reverse the molecular changes contributing to accelerated cardiac dysfunction in diabetic patients. Numerous animal models have been generated, which serve as powerful tools to study the impact of type 1 and type 2 diabetes on the heart. Despite specific limitations of the models generated, they mimic various perturbations observed in the diabetic myocardium and continue to provide important mechanistic insight into the pathogenesis underlying diabetic cardiomyopathy. This article reviews recent studies in both diabetic patients and in these animal models, and discusses novel hypotheses to delineate the increased incidence of heart failure in diabetic patients.
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Riehle et al. (2018) studied this question.
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