Key result
Carvedilol preserves cardiac function against doxorubicin-induced cell death via cardioprotective autophagy across experimental models.
Why the study?
Clinical trials evaluating whether carvedilol provides cardioprotection in cancer therapy-induced heart failure have generated mixed results that may depend on cancer regimens, tumors, or comorbidities.
Does carvedilol prevent doxorubicin-induced cardiotoxicity in in vitro and in vivo models?
Does carvedilol prevent doxorubicin-induced cardiotoxicity in in vitro and in vivo models?
Carvedilol demonstrates cardioprotective effects against doxorubicin-induced toxicity across multiple species in vitro and in vivo by restoring autophagy and mitochondrial energetics.
Background/Objectives: Carvedilol is an adrenergic blocker FDA-approved to improve outcomes in heart failure with reduced ejection fraction. Clinical trials examining whether carvedilol may be cardioprotective in the setting of cancer therapy-induced heart failure have generated mixed results that may depend on the cancer regimen, tumor, or comorbidities. Methods: To investigate the therapeutic potential of carvedilol to mitigate doxorubicin cardiotoxicity in cardiomyocytes, myocardial tissue, and in vivo, independent of confounding factors in clinical studies, we utilized disease-free cardiac slices and cardiomyocytes from mice, dogs, and human in vitro, and in wildtype mice injected with doxorubicin in vivo. We further evaluated the impact of carvedilol in dogs with cancer receiving doxorubicin. Results: In primary canine and murine cardiac slices, carvedilol treatment restored autophagy and prevented apoptosis from doxorubicin. Carvedilol restored mitochondrial energetics in human, canine, and murine models. In wildtype mice challenged with doxorubicin, carvedilol prevented declines in cardiac function and alterations in cardiac structure. In pet dogs with cancer and undergoing doxorubicin treatment, carvedilol was beneficial in preserving cardiac function and structure. Conclusions: Carvedilol activates cardioprotective autophagy, arrests doxorubicin-induced cell death, and improves energetics and cardiac structure and function across species.
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Boukhalfa et al. (2026) studied Doxorubicin cardiotoxicity. Carvedilol vs. Doxorubicin alone was evaluated on Cardiac function, structure, autophagy, and energetics. Carvedilol activated cardioprotective autophagy, arrested doxorubicin-induced cell death, and preserved cardiac structure and function across murine, canine, and human models.
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