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Autophagy contributes to retardation of cardiac growth in diabetic rats
Youngjeon Lee1, Yunkyung Hong, Sang-Rae Lee
1Department of Rehabilitation Science in Interdisciplinary PhD Program, Graduate School of Inje University, Gimhae, Korea.
Insights
High glucose impairs heart cell viability and activates autophagy, a cellular process implicated in the progression of diabetic cardiomyopathy in juvenile patients. This study investigates the role of autophagy in diabetes-induced heart disease.
Area of Science:
- Cardiology
- Endocrinology
- Cell Biology
Background:
- Diabetes mellitus is a significant risk factor for heart failure.
- The precise mechanisms linking diabetes to cardiomyopathy remain unclear.
Purpose of the Study:
- To investigate if prolonged high glucose exposure in cardiomyocytes induces autophagy.
- To determine the contribution of autophagy to diabetic cardiomyopathy.
Main Methods:
- In vitro studies exposing cardiomyocytes to varying glucose concentrations.
- In vivo studies using diabetic rat models.
- Analysis of microtubule-associated protein light chain 3 (LC3) expression and left ventricle (LV) size.
Main Results:
- High glucose concentrations reduced cardiomyocyte viability but did not alter autophagic activation.
- Diabetic rats exhibited increased LC3 expression and reduced LV size, indicating activated autophagy.
- Hyperglycemic oxidative stress was identified as an inducer of autophagy in vitro.
Conclusions:
- Autophagy is activated by hyperglycemic oxidative stress.
- Autophagy plays a role in the pathophysiological remodeling of the heart in diabetic cardiomyopathy.
- The findings suggest autophagy's involvement in the pathogenesis of juvenile diabetic cardiomyopathy.
Abstract:
Diabetes mellitus is a major predictor of heart failure, although the mechanisms by which the disease causes cardiomyopathy are not well understood. The purpose of this study was to determine whether prolonged exposure of cardiomyocytes to high glucose concentrations induces autophagy and contributes to cardiomyopathy. Interestingly, there were no differences in the autophagic activation produced by different glucose concentrations. However, cell viability was decreased by high glucose. In the diabetic rats, we found a higher level of microtubule-associated protein light chain 3 (LC3) expression and a reduction in the size of the left ventricle (LV) (P<0.05) caused by growth retardation, suggesting activated autophagy. Our in vitro findings indicate that hyperglycemic oxidative stress induces autophagy, and our in vivo studies reveal that autophagy is involved in the progression of pathophysiological remodeling of the heart. Taken together, the studies suggest that autophagy may play a role in the pathogenesis of juvenile diabetic cardiomyopathy.
