Why the study?
Hyperglycemia-induced oxidative stress leads to cardiomyocyte hypoxia and HIF-1α dysregulation, exacerbating diabetic myocardial injury, but the protective effects and mechanisms of the HIF-PHD inhibitor roxadustat (FG-4592) remain to be explored.
Does Roxadustat improve diabetic myocardial injury in preclinical models?
Population
Diabetic myocardial injury mice and high glucose-induced rat cardiomyocyte models
Comparison
FG-4592 pretreatment vs unexposed models
Design
Preclinical animal and cellular experimental study
Key result
Roxadustat exerted protective effects against diabetic myocardial injury in mice by reducing oxidative stress through the upregulation of HIF-1α and UCP2 and activation of the PI3K/AKT/Nrf2 pathway.
Authors
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Roxadustat may attenuate diabetic myocardial injury via HIF-1α; leaves open clinical translation in humans.
Does Roxadustat improve diabetic myocardial injury in preclinical models?
Roxadustat protects against diabetic myocardial injury in preclinical models by reducing oxidative stress through the HIF-1α/UCP2 and PI3K/AKT/Nrf2 pathways.
Fang et al. (2025) studied Diabetic myocardial injury (n=38). Roxadustat (FG-4592) vs. Vehicle (double-distilled water) was evaluated on Myocardial oxidative stress and mitochondrial function. Roxadustat exerted protective effects against diabetic myocardial injury in mice by reducing oxidative stress through the upregulation of HIF-1α and UCP2 and activation of the PI3K/AKT/Nrf2 pathway.
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