Publication | Closed Access

HDAC11 deletion reduces fructose-induced cardiac dyslipidemia, apoptosis and inflammation by attenuating oxidative stress injury

InflammationMetabolic SyndromeOxysterolCardiovascular DiseaseBiochemistryOxidative Stress InjuryHdac11 DeletionMedicineLipid PeroxidationCell DeathFructose-induced Cardiac DyslipidemiaReactive Oxygen SpeciePharmacologyCell BiologyRedox BiologyOxidative Stress