Niemann-Pick C1-Like 1 protein: Another target for treatment of dyslipidemia? Evidence from the Myocardial Infarction Genetic Consortium and IMPROVE-IT trials

Abstract

[first paragraph of article]

Absorption of both dietary cholesterol and cholesterol cleared from the liver through biliary secretion contributes substantially to tight control of cholesterol homeostasis. This process is mediated by a specific transporter – Niemann-Pick C1-Like 1 (NPC1L1) protein – localized to the brush border membrane of jejunal enterocytes (Figure 1, Table 1). NPC1L1 was first described by Davies and colleagues in 2000 while searching for proteins homologues of human Niemann-Pick type C1 protein (NPC1) – the primary causative protein for Niemann-Pick disease type C1 – that may be involved in subcellular cholesterol trafficking. Human liver express also NPC1L1, however its physiological significance in hepatocytes remains to be elucidated.