Pharmacological reactivation of autophagic flux by natural compounds or synthetic cell-permeable peptide prevents doxorubicin-induced cardiomyopathy

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Doxorubicin (DOX) is a potent chemotherapy agent that can cause cardiomyopathy in nearly 30% of patients within five years.
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Autophagy impairment is a recognized mechanism contributing to DOX-induced cardiomyopathy, suggesting that enhancing autophagy may mitigate cardiac damage.
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Trehalose (TRE) and spermidine (SP) are FDA-approved supplements that activate autophagy and have shown protective effects against cardiovascular diseases.
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This study investigates the effects of TRE, SP, and the synthetic peptide Tat-Beclin 1 D11 on cardiac function in a murine model of DOX-induced cardiomyopathy.
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The research aims to determine whether these agents interfere with DOX's antitumor activity while enhancing cardiac health in cancer patients.

Basic Research In Cardiology (Springer)

by Leonardo Schirone, Daniele Vecchio, Valentina Valenti, Vittorio Picchio, Sonia Schiavon, Luca D’Ambrosio, Flavio di Nonno, Selenia Miglietta, Michela Relucenti, Luca Madaro, Silvia Palmerio, Claudia Cozzolino, Margherita Litterio, Gianmarco Sarto, Beatrice Simeone, Nicola Moro, Shazia Tahir, Tania Zaglia, Giuseppe Biondi Zoccai, Elena De Falco, Vincenzo Petrozza, Ernesto Greco, Giacomo Frati, Maurizio Forte, Sebastiano Sciarretta
March 29, 2026

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