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Silencing of CD40 in vivo reduces progression of experimental atherogenesis through an NF-κB/miR-125b axis and reveals new potential mediators in the pathogenesis of atherosclerosis

Vascular DiseaseImmune RegulationImmunologyPathologyNew Potential MediatorsImmune SystemVivo Reduces ProgressionImmune DysregulationInflammationCardiovascular Disease PathogenesisAtherosclerosisCell SignalingMolecular SignalingChronic InflammationVascular BiologyImmune FunctionCell BiologyNf-κb/mir-125b AxisImmune Cell DevelopmentEndothelial DysfunctionMedicine