Molecular alterations of a protein begin in the diabetic heart from an early stage of the disease, before any clinically identifiable symptoms.

For the study, the researchers used the type-2 diabetic mouse model and matched around 35 such diabetic patients to comparable non-diabetic ones. The findings revealed markedly increased autophagy in the diabetic patients' heart tissues compared to the non-diabetic ones. This increase then triggered activation of pro-cell death proteins, which lead to progressive loss of cardiac cells. As more cells die, cardiac dysfunction develops and heart failure ensues.
Researchers also identified that diabetes increases autophagy through activation of the protein (Beclin-1). Katare said, "The protein presented an extremely promising target for new treatments of diabetes-related cardiac disease. We found that these molecular alterations begun in the diabetic heart from an early stage of the disease, before any clinically identifiable symptoms, so blocking them could be useful in combating cardiovascular complications in diabetes."
The study appeared in the International Journal of Cardiology.
Source-ANI
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