Key result
Venetoclax impairs cardiac function and cardiolipin composition in preclinical models.
Why the study?
Emerging clinical and preclinical evidence indicates that venetoclax therapy is associated with increased major adverse cardiovascular events, including heart failure and arrhythmias, with potential mitochondrial dysfunction.
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Alerts clinicians to potential venetoclax cardiotoxicity in leukemia; extends mechanistic insights but leaves open human translation.
Objectives: Venetoclax (VTX) has significantly improved outcomes for patients with acute myeloid leukemia (AML). However, emerging clinical and preclinical evidence indicates that VTX therapy is associated with increased major adverse cardiovascular events, including heart failure and arrhythmias. Preliminary results indicate that VTX reduces cardiomyocyte viability, impairs cardiac output and stroke volume, and alters cardiac cardiolipin composition, suggesting mitochondrial dysfunction. The objective of this study was to evaluate VTX-induced cardiotoxicity in mice, with a particular focus on mitochondrial cardiolipin remodeling.
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Kalhori et al. (2026) studied Venetoclax-induced cardiotoxicity. Venetoclax was evaluated on Mitochondrial cardiolipin remodeling and cardiotoxicity. Preliminary results indicate that venetoclax reduces cardiomyocyte viability, impairs cardiac output and stroke volume, and alters cardiac cardiolipin composition in mice.
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