Key result
Diabetes and hyperglycemia contribute to heart failure and diabetic cardiomyopathy through mechanisms including apoptosis and autophagic degeneration of cardiomyocytes.
This review highlights the potential role of cardiomyocyte apoptosis and autophagic degeneration in the pathogenesis of heart failure associated with diabetes.
Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. Furthermore, hyperglycemia as a sole risk factor may directly cause cardiovascular damage and lead to a complication such as diabetic cardiomyopathy. Alterations in myocardial structure and function occur during the late stage of diabetes. These chronic alterations are believed to result from acute cardiac responses to suddenly increased glucose levels at the early stage of diabetes. In failing hearts, cardiomyocytes degenerate and interstitial fibrosis, which indicates cardiomyocyte loss, becomes more prominent in the myocardium. Various mechanisms may establish an association of diabetes mellitus and heart failure as follows: first, comorbidities such as hypertension may play a role, diabetes also accelerates the development of coronary atherosclerosis, and experimental, clinical studies support the existence of microangiopathy, metabolic factors, or myocardial fibrosis influencing diabetic cardiomyopathy. Apoptosis of adult cardiac muscle cells can have lasting adverse consequences on overall cardiac performance. It is possible that autophagic degeneration may also be one of the mechanisms of myocardial cell death.
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Bhuvaneshwari et al. (2019) conducted a review in Heart failure associated with diabetes. Diabetes mellitus was evaluated. Diabetes and hyperglycemia contribute to heart failure and diabetic cardiomyopathy through mechanisms including apoptosis and autophagic degeneration of cardiomyocytes.
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