ATG5 and fibrosis: The results indicated that ATG5 knockdown by rAAV9-shRNA-ATG5 in mice for 7 weeks alleviated DOX-induced cardiac dysfunction, cardiac fibrosis, oxidative stress, and myocardial apoptosis (Figures 3B, 4A), and ATG5 overexpression by rAAV9-ATG5 exerted the opposite effects.