CCL2 and hyperlipidemia: During atherogenesis, primarily classical monocytes adhere to the endothelium to contribute to lesion development, likely due to their increased mobilization into the circulation during hyperlipidemia, which is mediated by the CCL2/CCR2 axis (already under steady state) and by the CXCL1/CXCR2 axis [31, 36, 37].