Why the study?
Doxorubicin use is limited by dose-dependent cardiotoxicity, and the cardioprotective effects and mechanisms of the Viscum coloratum-isolated compound DHDK remain unexplored.
Does DHDK protect against doxorubicin-induced cardiotoxicity in preclinical models?
Population
DOX-injured H9c2 cardiomyocytes and an in vivo rat model
Comparison
DHDK treatment vs DOX injury
Design
Preclinical in vitro and in vivo study
Key result
DHDK alleviated doxorubicin-induced cardiomyocyte toxicity by activating the PPARG-CPT1B-FAO axis and correcting lipid metabolic disorders in vitro and in an in vivo rat model.
Authors
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Supports further study of DHDK for DOX cardioprotection; leaves open human translation and should not yet change practice.
Does DHDK protect against doxorubicin-induced cardiotoxicity in preclinical models?
DHDK demonstrates preclinical potential as a cardioprotective agent against doxorubicin-induced cardiotoxicity by modulating lipid metabolism via the PPARG-CPT1B-FAO axis.
Hong et al. (2025) studied Doxorubicin-induced cardiotoxicity. DHDK was evaluated on Doxorubicin-induced cardiomyocyte toxicity. DHDK alleviated doxorubicin-induced cardiomyocyte toxicity by activating the PPARG-CPT1B-FAO axis and correcting lipid metabolic disorders in vitro and in an in vivo rat model.
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