Pharmacological reactivation of autophagic flux by natural compounds or synthetic cell-permeable peptide prevents doxorubicin-induced cardiomyopathy - PubMed
4 hours ago
- #Autophagy
- #Cardiotoxicity
- #Doxorubicin
- Doxorubicin (DOX)-induced cardiomyopathy is limited by incomplete understanding of its mechanisms.
- Restoring autophagic flux with natural (trehalose, spermidine) or synthetic (Tat-Beclin 1 D11) activators rescues cardiac function and reduces cardiotoxicity in mice.
- These autophagy activators preserve antineoplastic effects of DOX in cancer models without interfering with treatment efficacy.
- Boosting autophagic flux is a viable therapeutic strategy to prevent anthracycline-induced heart damage.