Figure 1.
(A) Hazard ratio by high-density lipoprotein cholesterol (HDL-C) quintile. (B) Correlation of HDL percentile with HDL-C level; red bar denotes the range for the “optimal” HDL-C level from A. MetS: metabolic syndrome; DysHDL: dysfunctional HDL
Figure 2.
Traditional reverse cholesterol transport model comprises three steps: (1) macrophage free cholesterol efflux to apolipoprotein AI via the ATP-binding cassette transporter A1 (ABCA1) yields nascent high-density lipoprotein (nHDL); (2) nHDL esterification by lecithin:cholesterol acyltransferase (LCAT) gives spherical HDL; and (3) selective hepatic uptake of HDL cholesterol ester. SR-B1: scavenger receptor class B type 1
Figure 3.
Cell free cholesterol (FC), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), and acyl-coenzyme A:cholesterol acyltransferase (ACAT) as a function of reassembled high-density lipoprotein (rHDL) mol% FC as labeled.
Figure 4.
Comparison of free cholesterol (FC) transfer from wild type (WT) and scavenger receptor class B type 1 (SR-B1)−/− high-density lipoprotein (HDL) mice. The initially higher mol% FC in SR-B1−/− versus WT HDL results in more transfer to LDL at equilibrium (t = 20 min). LP: lipoprotein; PL: phospholipid
Figure 5.
A revised reverse cholesterol transfer (RCT) model. In this model, (1) free cholesterol (FC) efflux to apolipoprotein AI (apoAI) via the ATP-binding cassette transporter A1 (ABCA1) forms nascent high-density lipoprotein (nHDL), which (2) transfers some of its FC to HDL within the plasma compartment (defined by the rectangle). (3, 4) FC transfers to the liver via scavenger receptor class B type 1 (SR-B1) and spontaneous transfer (5) and to erythrocytes. Concurrently, (6) some apoAI is released from nHDL and HDL for another cycle of efflux. PL: phospholipid