Specifically, SR-717 administration aggravated cardiac insufficiency in DOX-treated GsdmeCKO mice (Figure S7I), and the attenuation of myocardial fibrosis, collagen deposition, and abnormal TGF-β/SMAD2/SMAD3 activation in DOX-treated GsdmeCKO mice was suppressed by SR-717 administration (Figure S7J and S7K). This evidence concerns the gene SMAD2 and Myocardial fibrosis.