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. Author manuscript; available in PMC: 2012 Apr 12.
Published in final edited form as: Clin Lipidol. 2010 Jun;5(6):793–809. doi: 10.2217/clp.10.73

Figure 1. Molecular targets discussed in this review for gene therapy of dyslipidemia.

Figure 1

TG-rich lipoproteins are secreted by the intestine as chylomicrons and the liver as VLDL particles. These particles undergo lipolysis in the circulation, thereby, delivering fatty acids to tissues. Chylomicron remnants and approximately half of VLDL remnants are taken up by the liver. The remainder of the VLDL remnants are further metabolized to cholesterol-rich LDL. HDL is formed in the circulation from lipid-poor apolipoproteins secreted by liver and intestine and from surface components sloughed during lipolysis of TG-rich lipoproteins. Shown in black are candidates for gene replacement, shown in green are candidates for gene inhibition as discussed in this review.

CETP: Cholesterol-ester transfer protein; DGAT: Diacylglycerol acyltransferase; EL: Endothelial lipase; IDL: Intermediate density lipoprotein; LDLR: LDL receptor; TG: Triglyceride.