HDL biology
CETP is among seven cholesterol-handling genes up-regulated in peripheral blood of coronary artery disease patients (Curr Issues Mol Biol 2023)
Original title: Differential Expression of Subsets of Genes Related to HDL Metabolism and Atherogenesis in the Peripheral Blood in Coronary Artery Disease
Comparing transcript levels of 24 HDL-metabolism genes and 41 atherosclerosis-related genes in peripheral blood mononuclear cells from 76 male patients with coronary artery disease (CAD) and 63 controls identified twenty-eight differentially expressed genes. Expression of the cholesterol transporters ALB, APOA1, and LCAT was down-regulated, while AMN, APOE, LDLR, LPL, PLTP, PRKACA, and cholesteryl ester transfer protein (CETP) were up-regulated. Systemic inflammation in CAD was evidenced by up-regulation of IL1B, TLR8, CXCL5, and TNFRSF1A. In CAD patients, reverse cholesterol transport efficiency was 73-79%, and both atheroprotective (via S100A8) and proatherogenic (via SREBF1, LCAT, PRKACG, PRKACB, and PRKCQ) gene-expression associations with HDL cholesterol were identified, suggesting these genes and pathways may be targets for CAD diagnosis and treatment.
Original abstract
Differential expression of genes (DEGs) in coronary artery disease (CAD) and the association between transcript level and high-density lipoprotein cholesterol (HDL-C) were studied with 76 male patients with CAD and 63 control patients. The transcript level of genes related to HDL metabolism (24 genes) and atherosclerosis-prone (41 genes) in RNA isolated from peripheral blood mononuclear cells was measured by real-time RT-PCR. Twenty-eight DEGs were identified. The expression of cholesterol transporters, ALB, APOA1, and LCAT was down-regulated, while the expression of AMN, APOE, LDLR, LPL, PLTP, PRKACA, and CETP was up-regulated. The systemic inflammation in CAD is evidenced by the up-regulation of IL1B, TLR8, CXCL5, and TNFRSF1A. For the controls, TLR8 and SOAT1 were negative predictors of the HDL-C level. For CAD patients, PRKACG, PRKCQ, and SREBF1 were positive predictors, while PRKACB, LCAT, and S100A8 were negative predictors. For CAD patients, the efficiency of reverse cholesterol transport is 73-79%, and intracellular free cholesterol seems to accumulate at hyperalphalipoproteinemia. Both atheroprotective (via S100A8) and proatherogenic (via SREBF1, LCAT, PRKACG, PRKACB, and PRKCQ) associations of gene expression with HDL-C determine HDL functionality in CAD patients. The selected key genes and involved pathways may represent HDL-specific targets for the diagnosis and treatment of CAD and atherosclerosis.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.