
Suppression of generalized autophagy leads to senescence in cardiomyocytes, contributing to cardiac dysfunction. Loss of autophagy function resulted in increased senescent cells and deteriorated heart function in mice. Senolytic treatment improved outcomes and autophagy reactivation in doxorubicin-treated hearts alleviated senescence and dysfunction. These findings highlight the direct link between autophagy suppression, cellular senescence, and impaired cardiac function.
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