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Methylglyoxal evokes acute Ca2+ transients in distinct cell types and increases agonist-evoked Ca2+ entry in endothelial cells via CRAC channels

Cardiovascular FunctionCellular PhysiologySocial SciencesOxidative StressAgonist-evoked Ca2+ EntryCell SignalingMolecular PhysiologyVascular BiologyPharmacologyCell BiologySignal TransductionNeurophysiologyPhysiologyEndothelial DysfunctionAcute Ca2+ TransientsElectrophysiologyCardiovascular PhysiologyMedicineCrac Channels