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Working model. Doxorubicin, by inhibiting lysosomal acidification and lysosomal function, blocks cardiomyocyte autophagic flux. Accumulation of autolysosomes leads to increased ROS production and cardiac injury. Slowing autophagy initiation by decreasing Beclin 1 partially rescues the autophagic flux blockage and protects heart from cardiotoxicity; conversely, increasing autophagosome formation exacerbates autophagic flux inhibition and increases doxorubicin cardiotoxicity.
