Fig. 4
From: Loss-of-function mutation in Pcsk1 increases serum APOA1 level and LCAT activity in mice
HDL biogenesis, remodeling and catabolism. APOA1 is predominantly produced in the liver and secreted into circulation as a lipid-free APOA1 precursor, which is subsequently converted to the mature APOA1 (APOA1 maturation). Initial APOA1 lipidation occurs by acquisition of phospholipids and unesterified cholesterol through phospholipid transfer protein (PLTP), leading to formation of lipid-poor HDL (also called pre-β-HDL). Further unesterified cholesterol conversion to cholesteryl ester happens through lecithin-cholesterol acyltransferase (LCAT), which turns the pre-β-HDL to a larger cholesterol-rich and triglyceride-containing HDL (also called α-HDL). APOA1 in the large α-HDL particles is released during HDL catabolism. The delipidated APOA1 is cleared through the kidney