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The discovery in 2003 that variants in the PCSK9 (proprotein convertase subtilisin/kexin type 9) gene cause autosomal dominant hypercholesterolemia revealed a new aspect of LDL cholesterol (LDL-C)2 metabolism (1). PCSK9, a protein of 692 amino acid residues produced at high concentrations in the liver, kidney, and intestine, has profound effects on LDL-C concentrations (2). Both gain-of-function and loss-of-function PCSK9 variants that cause higher and lower LDL-C concentrations, respectively, have been described, and variants in PCSK9 contribute to population variation in LDL-C values (3). The mechanism by which PCSK9 affects LDL-C concentrations involves direct binding of the protein to epidermal growth factor–like repeat A in the extracellular domain of the LDL receptor (LDLR), thereby accelerating degradation of the receptor (4).PCSK9 is a secreted protein that circulates in the blood. Several ELISA assays have been developed to measure PCSK9 concentrations (5, 6) and relate them to various biological correlates and differences in response to therapy, which may have implications for the therapeutic targeting of this protein.The interactions of statins with PCSK9 are of great interest, not only because statins are the predominant therapeutic agents used to decrease LDL-C but also because both the LDLR and PCSK9 share a common transcriptional regulator, sterol regulator element–binding protein 2 (SREBP-2) (7). Statin exposure produces an increase in the concentrations of both LDLR and PCSK9 mRNAs. The upregulation of PCSK9, which promotes the degradation of the LDLR, serves as a counterregulatory molecular brake on LDL-C lowering. The study described by Awan et al. (8) in …

Statins, Plasma Proprotein Convertase Subtilisin/Kexin Type 9 Concentrations, and LDL Lowering