Key result
Carvedilol pretreatment preserves mitochondrial respiration and prevents doxorubicin-induced cardiotoxicity in human iPSC-CMs.
Why the study?
Anthracycline doxorubicin causes dose-related cardiotoxicity through mitochondrial dysfunction, and mechanisms of cardioprotection by carvedilol and enalapril remain poorly understood.
Does pretreatment with carvedilol or enalapril prevent doxorubicin-induced mitochondrial dysfunction in cardiomyocytes?
Does pretreatment with carvedilol or enalapril prevent doxorubicin-induced mitochondrial dysfunction in cardiomyocytes?
Carvedilol pretreatment mitigates doxorubicin-induced mitochondrial dysfunction in human iPSC-derived cardiomyocytes, providing a potential mechanism for its cardioprotective effects in anthracycline therapy.
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Unchecked mitochondrial fission and mitophagy mediate doxorubicin cardiomyocyte death; leaves open whether DRP1 or parkin inhibition reduces clinical cardiotoxicity.
Uche et al. (2022) studied Doxorubicin-induced cardiotoxicity. Carvedilol or enalapril pretreatment vs. Doxorubicin alone was evaluated on Mitochondrial respiration (oxygen consumption rates) and mitochondrial content. Carvedilol pretreatment significantly improved maximal oxygen consumption rates and prevented doxorubicin-induced suppression of mitochondrial function in human iPSC-CMs compared to doxorubicin alone.
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