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

•Silencing CD40 in ApoE–/– mice reduced atherosclerotic lesions, number of macrophages and NF-κB positive cells in the intima.•Xpr1, Taf3, Riken cDNA1700017N19, miR-30a and miR-125b were overexpressed during atherosclerosis progression.•XPR1 and TAF3 were identified in human plaques, and mainly localized in the perivascular adipose tissue (PVAT).•Expression of miR-125b is under the control of the CD40 and NF-κB signaling pathways.