Figure 1.

Overview of synthesis, maturation, and disposal of high-density lipoproteins (HDLs). Apolipoprotein A1 (apoA1) is synthesized by the action of ATP-binding cassette transporter AI (ABCA1) in the liver and small intestine and is secreted as immature HDL (imm HDL) particles with large amounts of protein and small amounts of free cholesterol. Macrophages and peripheral tissues also donate free cholesterol and phospholipids to apoA1 to form more immature HDL particles. The action of lecithin cholesterol acyltransferase (LCAT) adds esterified cholesterol to the core of HDLs, leading to mature HDL particles composed of lipoproteins (apoA1 being the most abundant), phospholipids, and cholesterol esters. Cholesterol esters are shuttled to apoB-rich low-density lipoproteins (LDLs) and very-low-density lipoproteins (VLDLs) by the actions of cholesterol ester transfer protein (CETP). Conversely, phospholipids are transferred from LDLs/VLDLs to HDLs by the action of phospholipid transfer protein (PLTP). HDLs, as they break down, donate phospholipids and cholesterol/cholesterol esters, which are bound by SR-B1 receptor on liver cells. LDLs are bound by LDL receptor (LDLR) on hepatocytes. ApoA1 can be reused or secreted by the liver. Cholesterol can be reused or secreted into the bile for disposal. Triangles = apoA1; diamond = apoB. CE, cholesterol esters; FC, free cholesterol; PL, phospholipids; TG, triglycerides. The figure is based, in part, on figures and data in [102] and [103].