20-Deoxyingenol attenuated doxorubicin-induced cardiotoxicity by promoting autolysosome degradation through the UCHL3-TFEB pathway
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Background: Impaired autophagic flux is an essential contributor to doxorubicin (DOX)-induced cardiotoxicity (DIC). TFEB is recognized as a key regulator of DOX-induced autolysosome accumulation; however, the mechanisms by which ... ...
