Disruption of MAP7D1 Gene Function Increases the Risk of Doxorubicin-Induced Cardiomyopathy and Heart Failure

Figure 4

Working model of MAP7D1 in doxorubicin-induced cardiomyopathy. Doxorubicin causes cardiotoxicity by inhibiting autolysosome formation, resulting in elevated ROS and cardiomyocyte apoptosis. Disruption of MAP7D1 protein function further impaired autophagosome formation and led to accumulation of toxic protein aggregation, thus exacerbating doxorubicin-induced cardiomyopathy and heart failure.