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ROS generated during early reperfusion contribute to intermittent hypobaric hypoxia-afforded cardioprotection against postischemia-induced Ca2+ overload and contractile dysfunction via the JAK2/STAT3 pathway

InflammationHeart FailureCardiovascular DiseaseEarly Reperfusion ContributeCell SignalingJak2/stat3 PathwayPhysiologyMedicineHypoxia (Medicine)AnesthesiologyReactive Oxygen SpecieReperfusion InjuryPostischemia-induced Ca2+ OverloadRedox BiologyOxidative Stress