LDLR and atherosclerosis: Increased CHOL uptake (in response to upregulation of NPC1L1, SR-B1, CD36 and LDLR) or decreased CHOL excretion (due to downregulation of ABCA1, ATP-binding cassette transporter G5/G8 and trans-intestinal CHOL excretion) can influence pathogenesis of hypercholesterolemia, DLP and atherosclerosis [39,40,41,42,43].