Dapagliflozin Attenuates Severity of Atherosclerosis through Manufacturing Energy-Crisis to Inhibit Ferroptosis of Macrophage

Background: Atherosclerosis is a main potential pathology of most cardiovascular diseases. Growing evidence has indicated that dysregulation ferroptosis associated with atherosclerosis. Dapagliflozinas sodiumglucose cotransporter 2 inhibitor (SGLT2i), in view the clinically important benefits sodium-glucose (SGLT2i) dapagliflozin improving outcomes, we aimed to explore its pharmacological effects and underlying mechanisms atherosclerosis ferroptosis. Method: Ferroptosis severity were assessed ApoE-/-(control) ApoE-/-+Dapagliflozin mice groups analyze changes after Dapagliflozin treatment. ApoE-/-+Dapagliflozin+RSL3 (RSL3) group was established confirm association between Metabolism nutrients energetic phenotype macrophages sorted by FACS within plaques analyzed mechanism attenuating Result: Alleviated observed treatment group, however, RSL3 revoke beneficial effect. The metabolism Fluorescence Activated Cell Sorter (FACS) weakened fuel flexibility mitochondrial respiration consumption which leads energy crisis macrophages. mitigates keeps more M2 surviving atherosclerotic plaques. Conclusion: treatments modulate plaque progression maintain stabilization way creating crisis. Energy sensitive than M1 attenuate might be new therapeutic medication target for lesions.