Key result
Sorafenib induced cardiomyocyte apoptosis and contractile dysfunction in zebrafish and rat models, an effect mitigated by alpha-adrenergic signaling activation.
Why the study?
Does sorafenib induce cardiotoxicity in preclinical models, and what are the underlying mechanisms?
Population
Zebrafish model and cultured rat cardiomyocytes
Comparison
Kinase inhibitors, adenovirus-mediated gene… vs Control/untreated models and non-cardiotoxic…
Design
Preclinical
Authors
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Zebrafish may enable rapid KI cardiotoxicity screening; leaves open mammalian validation and clinical translation.
Does sorafenib induce cardiotoxicity in preclinical models, and what are the underlying mechanisms?
Zebrafish serve as a valuable preclinical model for predicting kinase inhibitor cardiotoxicity, revealing that sorafenib-induced cardiomyopathy is modulated by the alpha-adrenergic signaling pathway.
Cheng et al. (2011) studied Cardiotoxicity. Sorafenib vs. Gefitinib and Sunitinib was evaluated on Cardiotoxicity (cardiomyocyte apoptosis, contractile dysfunction, ventricular dilatation). Sorafenib induced cardiomyocyte apoptosis and contractile dysfunction in zebrafish and rat models, an effect mitigated by alpha-adrenergic signaling activation.
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