Diabetes mellitus increases the risk of atherosclerotic plaques formation in the coronary arteries, which eventually results in the blockage of blood supply to the heart causing heart attacks.
Moreover, diabetes stresses the cardiac cells directly leading to precocious senescence of the heart, a condition called as diabetic cardiomyopathy.
If left untreated diabetic cardiomyopathy leads to progressive deterioration of heart functions resulting in the development of heart failure.
The underlying cellular and molecular mechanisms mediating this progression are still unknown.
In this context, we aim to demonstrate the key role of autophagy in mediating the progression of cardiomyopathy to heart failure.
Autophagy is a mechanism used normally by the cells to recycle the waste material.
Our initial results showed that this mechanism becomes inefficient in the diabetic heart leading to accumulation of toxic products and cell death (Figure).
Using animal models of diabetic heart disease, we will study the development of suicidal autophagy (autophagy associated with cell death) in diabetic hearts through measurement of the expression levels of genes which regulate autophagy.
Positive results from this study will enlighten a new mechanism for the development of cardiac complications in diabetic patients and will therefore help in formulation of new specific therapies for the treatment of diabetic heart disease.