Fig. 1
From: PCSK9 inhibition and cholesterol homeostasis in insulin producing β-cells
Schematic overview of cellular regulation of PCSK9 expression, processing, secretion, interaction with LDLR and degradation. (1) Gene expression of both PCSK9 and LDLR is induced by SREBP-2. (2) After maturation in the Golgi, PCSK9 is either routed to exocytosis or is intended together with LDLR to degradation in lysosomes. (3) LDL binds LDLR and both will be internalized. LDLR will be recycled if it is not bound to PCSK and thereby marked for degradation. (4) PCSK9 inhibits the expression of ABCA1, which together with ABCG1 exports intracellular surplus cholesterol to HDL formation in the blood stream and subsequent RCT to liver or TICE. (5) Cholesterol can also be excreted to bile or intestine via ABCG5/ABCG8 and ABCB1a/b. As alternative LDL-lowering drugs, (5) ezetimibe inhibits NPC1L1-mediated cholesterol uptake from intestine and (6) statins inhibit HMGCR-mediated cholesterol synthesis. The figure contains elements from Smart Servier Medical Arts (https://smart.servier.com/category/cellular-biology/intracellular-components/)