Publication | Open Access

Impaired cytosolic NADH shuttling and elevated UCP3 contribute to inefficient citric acid cycle flux support of postischemic cardiac work in diabetic hearts

Metabolic SyndromePostischemic Cardiac WorkUcp3 ContributeMolecular PhysiologyDiabetic HeartsBiochemistryCardiac MusclePhysiologyDiabetesMetabolic RemodelingCardiovascular PhysiologyCardiovascular FunctionMetabolismMedicineCell BiologyCardiologyOxidative StressHealth Sciences