Published in the Journal of Clinical Investigation by Dr. The study, led by Paul Shumaker, shows that inhibiting the UQCRFS1 gene causes adult cardiomyocytes to revert to an embryonic-like state, allowing them to regenerate and use glucose in the same way as the embryonic heart. cells.
This approach could pave the way for treating hypoplastic left heart syndrome (HLHS) in children and repairing heart damage in adults. HLHS is a serious birth defect that occurs in 1 in 5,000 births and often leads to premature death. The findings suggest that stimulating glucose utilization in heart cells can restore the cells’ ability to divide and grow.
Schumaker and his team are now focused on finding drugs that could mimic this genetic manipulation and offer a potential noninvasive treatment. This advance promises restoration of normal heart function in children with HLHS and adults who have had heart attacks.
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Source: Ferra
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