Fig. 8From: Asprosin inhibits macrophage lipid accumulation and reduces atherosclerotic burden by up-regulating ABCA1 and ABCG1 expression via the p38/Elk-1 pathwayA model describing the mechanism for asprosin-induced atheroprotection. Asprosin activates p38 and then phosphorylates Elk-1 at Ser383. After phosphorylation, Elk-1 enters the nucleus to stimulate ABCA1 and ABCG1 transcription. Increased ABCA1 and ABCG1 expression promotes cholesterol efflux from macrophages, leading to acceleration of RCT and alleviation of atherosclerotic plaque burdenBack to article page