Reverse cholesterol transport pathway

Reverse cholesterol transport (RCT) is a crucial physiological pathway for removal of excess cholesterol from peripheral tissues, especially cholesterol-loaded macrophages, and its delivery to the liver for excretion in bile. Key molecular participants include apolipoprotein A-I, ATP-binding cassette transporters ABCA1 and ABCG1, scavenger receptor class B type 1 (SR-B1), lecithin-cholesterol acyltransferase (LCAT), and the nuclear receptor LXR[1][8]. The process is initiated when cholesterol from macrophage foam cells is effluxed, transferred to HDL particles, esterified, and ultimately cleared via hepatic uptake and biliary excretion[5][7]. Dysfunction or impairment of RCT is mechanistically linked to atherosclerosis and cardiovascular disease, and the pathway is frequently discussed as a therapeutic target for modulation, but it does not correspond to a single molecular entity that can be directly targeted[3][7]. Drugs in development or use typically target specific proteins or receptors (e.g., ABCA1, LXR, CETP), rather than the abstract pathway as a whole[2][6]. Note: In structured data systems, the correct approach is to map "Reverse cholesterol transport pathway" to the constituent molecular targets (e.g., ABCA1, ABCG1, LCAT, SR-B1, LXR) for annotations of drugs, disease roles, mechanisms, and safety concerns[2][6][8].

Other names

RCT pathwayReverse cholesterol transportHDL-mediated cholesterol efflux

Enhancement of HDL-mediated cholesterol efflux, Upregulation of ABCA1/ABCG1 expression, Activation of LXR nuclear receptor signaling, Inhibition of miR-33 microRNA to increase ABCA1