Why the study?
Doxorubicin cardiotoxicity limits its clinical use, but the role of roxadustat (FG-4592) in doxorubicin-induced cardiotoxicity was unknown.
Does roxadustat (FG-4592) pretreatment prevent doxorubicin-induced cardiotoxicity in preclinical models?
Population
Mice, rat cardiomyocyte cells (H9c2), and HepG2 and MCF-7 cell lines
Comparison
DOX with FG-4592 pretreatment vs DOX alone, FG-4592 alone, and control
Design
In vivo animal and in vitro cell experimental study
Key result
Roxadustat (FG-4592) alleviated doxorubicin-induced cardiotoxicity in mice by protecting against cardiac dysfunction, apoptosis, and oxidative stress via upregulation of HIF-1α.
Authors
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May inform cardioprotection trials during chemotherapy; leaves open translation from murine models to patients.
Does roxadustat (FG-4592) pretreatment prevent doxorubicin-induced cardiotoxicity in preclinical models?
Roxadustat (FG-4592) protects against doxorubicin-induced cardiotoxicity in preclinical models by activating HIF-1a and its antiapoptotic and antioxidative target genes, without compromising doxorubicin's antitumor efficacy.
Long et al. (2020) studied Doxorubicin-induced cardiotoxicity (n=23). Roxadustat (FG-4592) vs. Doxorubicin alone was evaluated on Cardiac function (LVEF and LVFS) and cardiomyocyte apoptosis. Roxadustat (FG-4592) alleviated doxorubicin-induced cardiotoxicity in mice by protecting against cardiac dysfunction, apoptosis, and oxidative stress via upregulation of HIF-1α.
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