In summary, the above-mentioned study showed that NEU1 promoted DRP1-dependent mitochondrial fission and mitophagy, which was a critical initiator of DOX-induced cardiomyopathy, but NEU1 inhibition mediated by its inhibitors such as OSE demonstrated novel cardio-protective effects against DOX-induced cardiotoxicity. Here, DNM1L is linked to cardiomyopathy.