Figure.

FOXP1 acts as a gatekeeper of endothelial inflammation. In areas where laminar flow is present the Krüppel-like factor 2 (KLF2) is expressed which in turn stimulates expression of FOXP1. FOXP1 suppresses the expression of components of the NLRP3-inflammasome and Ccl8. In areas of disturbed flow, which also develops atherosclerosis, FOXP1 levels are reduced allowing for increased expression of inflammasome components and chemokines. Disturbed flow triggers expression of SREBP2 (sterol regulatory element binding protein 2) which increases cholesterol accumulation which might act as the second signal to activate the NLRP3 inflammasome. Also, dyslipidemia induces cholesterol crystal formation which might further activate the inflammasome in endothelial cells. All of which results in increased monocyte recruitment and acceleration of atherosclerosis.