100
Views
7
CrossRef citations to date
0
Altmetric
Theme: Lipoprotein Disorders - Review

Pharmacogenomics of high-density lipoprotein-cholesterol-raising therapies

, , , &
Pages 355-364 | Published online: 10 Jan 2014

References

  • Cannon CP. High-density lipoprotein cholesterol as the Holy Grail. JAMA 306(19), 2153–2155 (2011).
  • Voight BF, Peloso GM, Orho-Melander M et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 380(9841), 572–580 (2012).
  • Rice T, Després JP, Pérusse L et al. Familial aggregation of blood lipid response to exercise training in the health, risk factors, exercise training, and genetics (HERITAGE) Family Study. Circulation 105(16), 1904–1908 (2002).
  • Goodarzi MO, Taylor KD, Scheuner MT et al. Haplotypes in the lipoprotein lipase gene influence high-density lipoprotein cholesterol response to statin therapy and progression of atherosclerosis in coronary artery bypass grafts. Pharmacogenomics J. 7(1), 66–73 (2007).
  • Blanche PJ, Gong EL, Forte TM, Nichols AV. Characterization of human high-density lipoproteins by gradient gel electrophoresis. Biochim. Biophys. Acta 665(3), 408–419 (1981).
  • Freedman DS, Otvos JD, Jeyarajah EJ, Barboriak JJ, Anderson AJ, Walker JA. Relation of lipoprotein subclasses as measured by proton nuclear magnetic resonance spectroscopy to coronary artery disease. Arterioscler. Thromb. Vasc. Biol. 18(7), 1046–1053 (1998).
  • Warnick GR. Measurement and clinical significance of high-density lipoprotein cholesterol subclasses. In: Handbook of Lipoprotein Testing. Rifai M, Warnick GR, Dominiczak MH (Eds). AACC Press, Washington, DC, USA, 251–266 (1997).
  • Duriez P, Fruchart JC. High-density lipoprotein subclasses and apolipoprotein A-I. Clin. Chim. Acta 286(1–2), 97–114 (1999).
  • Otvos JD, Collins D, Freedman DS et al. Low-density lipoprotein and high-density lipoprotein particle subclasses predict coronary events and are favorably changed by gemfibrozil therapy in the Veterans Affairs High-Density Lipoprotein Intervention Trial. Circulation 113(12), 1556–1563 (2006).
  • Natarajan P, Ray KK, Cannon CP. High-density lipoprotein and coronary heart disease: current and future therapies. J. Am. Coll. Cardiol. 55(13), 1283–1299 (2010).
  • Guyton JR, Blazing MA, Hagar J et al. Extended-release niacin vs gemfibrozil for the treatment of low levels of high-density lipoprotein cholesterol. Niaspan-Gemfibrozil Study Group. Arch. Intern. Med. 160(8), 1177–1184 (2000).
  • Digby JE, Ruparelia N, Choudhury RP. Niacin in cardiovascular disease: recent preclinical and clinical developments. Arterioscler. Thromb. Vasc. Biol. 32(3), 582–588 (2012).
  • Lukasova M, Malaval C, Gille A, Kero J, Offermanns S. Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells. J. Clin. Invest. 121(3), 1163–1173 (2011).
  • Pike NB. Flushing out the role of GPR109A (HM74A) in the clinical efficacy of nicotinic acid. J. Clin. Invest. 115(12), 3400–3403 (2005).
  • Kamanna VS, Kashyap ML. Mechanism of action of niacin. Am. J. Cardiol. 101(8A), 20B–26B (2008).
  • Sakai T, Kamanna VS, Kashyap ML. Niacin, but not gemfibrozil, selectively increases LP-AI, a cardioprotective subfraction of HDL, in patients with low HDL cholesterol. Arterioscler. Thromb. Vasc. Biol. 21(11), 1783–1789 (2001).
  • Zhang LH, Kamanna VS, Ganji SH, Xiong XM, Kashyap ML. Niacin increases HDL biogenesis by enhancing DR4-dependent transcription of ABCA1 and lipidation of apolipoprotein A-I in HepG2 cells. J. Lipid Res. 53(5), 941–950 (2012).
  • Wu ZH, Zhao SP. Niacin promotes cholesterol efflux through stimulation of the PPARγ-LXRα-ABCA1 pathway in 3T3-L1 adipocytes. Pharmacology 84(5), 282–287 (2009).
  • Lin SH, Liu CM, Chang SS et al. Familial aggregation in skin flush response to niacin patch among schizophrenic patients and their nonpsychotic relatives. Schizophr. Bull. 33(1), 174–182 (2007).
  • Katherisan S, Rader DJ. Lipoprotein disorders. In: Essentials of Genomic and Personalized Medicine. Ginsburg GS, Willard H (Eds). Academic Press, Burlington, MA, USA, 269–281 (2010).
  • van der Hoorn JW, de Haan W, Berbée JF et al. Niacin increases HDL by reducing hepatic expression and plasma levels of cholesteryl ester transfer protein in APOE*3Leiden.CETP mice. Arterioscler. Thromb. Vasc. Biol. 28(11), 2016–2022 (2008).
  • Hertz R, Bishara-Shieban J, Bar-Tana J. Mode of action of peroxisome proliferators as hypolipidemic drugs. Suppression of apolipoprotein C-III. J. Biol. Chem. 270(22), 13470–13475 (1995).
  • Hossain MA, Tsujita M, Gonzalez FJ, Yokoyama S. Effects of fibrate drugs on expression of ABCA1 and HDL biogenesis in hepatocytes. J. Cardiovasc. Pharmacol. 51(3), 258–266 (2008).
  • van der Hoogt CC, de Haan W, Westerterp M et al. Fenofibrate increases HDL-cholesterol by reducing cholesteryl ester transfer protein expression. J. Lipid Res. 48(8), 1763–1771 (2007).
  • Berthou L, Duverger N, Emmanuel F et al. Opposite regulation of human versus mouse apolipoprotein A-I by fibrates in human apolipoprotein A-I transgenic mice. J. Clin. Invest. 97(11), 2408–2416 (1996).
  • Guérin M, Bruckert E, Dolphin PJ, Turpin G, Chapman MJ. Fenofibrate reduces plasma cholesteryl ester transfer from HDL to VLDL and normalizes the atherogenic, dense LDL profile in combined hyperlipidemia. Arterioscler. Thromb. Vasc. Biol. 16(6), 763–772 (1996).
  • Lai CQ, Parnell LD, Ordovas JM. The APOA1/C3/A4/A5 gene cluster, lipid metabolism and cardiovascular disease risk. Curr. Opin. Lipidol. 16(2), 153–166 (2005).
  • Vu-Dac N, Gervois P, Jakel H et al. Apolipoprotein A5, a crucial determinant of plasma triglyceride levels, is highly responsive to peroxisome proliferator-activated receptor alpha activators. J. Biol. Chem. 278(20), 17982–17985 (2003).
  • Lai CQ, Arnett DK, Corella D et al. Fenofibrate effect on triglyceride and postprandial response of apolipoprotein A5 variants: the GOLDN study. Arterioscler. Thromb. Vasc. Biol. 27(6), 1417–1425 (2007).
  • Liu Y, Ordovas JM, Gao G et al. Pharmacogenetic association of the APOA1/C3/A4/A5 gene cluster and lipid responses to fenofibrate: the genetics of lipid-lowering drugs and diet network study. Pharmacogenet. Genomics 19(2), 161–169 (2009).
  • Brautbar A, Covarrubias D, Belmont J et al. Variants in the APOA5 gene region and the response to combination therapy with statins and fenofibric acid in a randomized clinical trial of individuals with mixed dyslipidemia. Atherosclerosis 219(2), 737–742 (2011).
  • Feitosa MF, An P, Ordovas JM et al. Association of gene variants with lipid levels in response to fenofibrate is influenced by metabolic syndrome status. Atherosclerosis 215(2), 435–439 (2011).
  • Brisson D, Ledoux K, Bossé Y et al. Effect of apolipoprotein E, peroxisome proliferator-activated receptor alpha and lipoprotein lipase gene mutations on the ability of fenofibrate to improve lipid profiles and reach clinical guideline targets among hypertriglyceridemic patients. Pharmacogenetics 12(4), 313–320 (2002).
  • Christidis DS, Liberopoulos EN, Kakafika AI et al. The effect of apolipoprotein E polymorphism on the response to lipid-lowering treatment with atorvastatin or fenofibrate. J. Cardiovasc. Pharmacol. Ther. 11(3), 211–221 (2006).
  • Tsai MY, Ordovas JM, Li N et al. Effect of fenofibrate therapy and ABCA1 polymorphisms on high-density lipoprotein subclasses in the genetics of lipid lowering drugs and diet network. Mol. Genet. Metab. 100(2), 118–122 (2010).
  • Bossé Y, Pascot A, Dumont M et al. Influences of the PPARα-L162V polymorphism on plasma HDL(2)-cholesterol response of abdominally obese men treated with gemfibrozil. Genet. Med. 4(4), 311–315 (2002).
  • Cresci S. Pharmacogenetics of the PPAR genes and cardiovascular disease. Pharmacogenomics 8(11), 1581–1595 (2007).
  • Tai ES, Collins D, Robins SJ et al. The L162V polymorphism at the peroxisome proliferator activated receptor alpha locus modulates the risk of cardiovascular events associated with insulin resistance and diabetes mellitus: the Veterans Affairs HDL Intervention Trial (VA-HIT). Atherosclerosis 187(1), 153–160 (2006).
  • Shen J, Arnett DK, Parnell LD et al. The effect of CYP7A1 polymorphisms on lipid responses to fenofibrate. J. Cardiovasc. Pharmacol. 59(3), 254–259 (2012).
  • Brousseau ME, Goldkamp AL, Collins D et al. Polymorphisms in the gene encoding lipoprotein lipase in men with low HDL-C and coronary heart disease: the Veterans Affairs HDL Intervention Trial. J. Lipid Res. 45(10), 1885–1891 (2004).
  • Frazier-Wood AC, Aslibekyan S, Borecki IB et al. Genome-wide association study indicates variants associated with insulin signaling and inflammation mediate lipoprotein responses to fenofibrate. Pharmacogenet. Genomics 22(10), 750–757 (2012).
  • Ziouzenkova O, Perrey S, Asatryan L et al. Lipolysis of triglyceride-rich lipoproteins generates PPAR ligands: evidence for an antiinflammatory role for lipoprotein lipase. Proc. Natl Acad. Sci. USA 100(5), 2730–2735 (2003).
  • Tojcic J, Benoit-Biancamano MO, Court MH, Straka RJ, Caron P, Guillemette C. In vitro glucuronidation of fenofibric acid by human UDP-glucuronosyltransferases and liver microsomes. Drug Metab. Dispos. 37(11), 2236–2243 (2009).
  • Arafah A, Guillemette C, Tsai MY, et al. Evidence of UGT2B7 as a pharmacogenetic determinant of variability in serum fenofibric acid in human subjects. Presented at: Arteriosclerosis, Thrombosis, and Vascular Biology Scientific Sessions. Chicago, IL, USA, 18–20 April 2012.
  • Kostapanos MS, Milionis HJ, Filippatos TD et al. Dose-dependent effect of rosuvastatin treatment on HDL-subfraction phenotype in patients with primary hyperlipidemia. J. Cardiovasc. Pharmacol. Ther. 14(1), 5–13 (2009).
  • Teramoto T. The clinical impact of pitavastatin: comparative studies with other statins on LDL-C and HDL-C. Expert Opin. Pharmacother. 13(6), 859–865 (2012).
  • Barter PJ, Brandrup-Wognsen G, Palmer MK, Nicholls SJ. Effect of statins on HDL-C: a complex process unrelated to changes in LDL-C: analysis of the VOYAGER Database. J. Lipid Res. 51(6), 1546–1553 (2010).
  • Postmus I, Verschuren JJ, de Craen AJ et al. Pharmacogenetics of statins: achievements, whole-genome analyses and future perspectives. Pharmacogenomics 13(7), 831–840 (2012).
  • Barber MJ, Mangravite LM, Hyde CL et al. Genome-wide association of lipid-lowering response to statins in combined study populations. PLoS ONE 5(3), e9763 (2010).
  • Poduri A, Khullar M, Bahl A, Sehrawat BS, Sharma Y, Talwar KK. Common variants of HMGCR, CETP, APOAI, ABCB1, CYP3A4, and CYP7A1 genes as predictors of lipid-lowering response to atorvastatin therapy. DNA Cell Biol. 29(10), 629–637 (2010).
  • Kajinami K, Brousseau ME, Ordovas JM, Schaefer EJ. CYP3A4 genotypes and plasma lipoprotein levels before and after treatment with atorvastatin in primary hypercholesterolemia. Am. J. Cardiol. 93(1), 104–107 (2004).
  • Gao Y, Zhang LR, Fu Q. CYP3A4*1G polymorphism is associated with lipid-lowering efficacy of atorvastatin but not of simvastatin. Eur. J. Clin. Pharmacol. 64(9), 877–882 (2008).
  • Fiegenbaum M, da Silveira FR, Van der Sand CR et al. The role of common variants of ABCB1, CYP3A4 and CYP3A5 genes in lipid-lowering efficacy and safety of simvastatin treatment. Clin. Pharmacol. Ther. 78(5), 551–558 (2005).
  • Rosales A, Alvear M, Cuevas A, Saavedra N, Zambrano T, Salazar LA. Identification of pharmacogenetic predictors of lipid-lowering response to atorvastatin in Chilean subjects with hypercholesterolemia. Clin. Chim. Acta 413(3–4), 495–501 (2012).
  • Wei KK, Zhang LR, Zhang Y, Hu XJ. Interactions between CYP7A1 A-204C and ABCG8 C1199A polymorphisms on lipid lowering with atorvastatin. J. Clin. Pharm. Ther. 36(6), 725–733 (2011).
  • Lahoz C, Peña R, Mostaza JM et al.; RAP Study Group. Apo A-I promoter polymorphism influences basal HDL-cholesterol and its response to pravastatin therapy. Atherosclerosis 168(2), 289–295 (2003).
  • Sorkin SC, Forestiero FJ, Hirata MH et al. APOA1 polymorphisms are associated with variations in serum triglyceride concentrations in hypercholesterolemic individuals. Clin. Chem. Lab. Med. 43(12), 1339–1345 (2005).
  • Hamrefors V, Orho-Melander M, Krauss RM et al. A gene score of nine LDL and HDL regulating genes is associated with fluvastatin-induced cholesterol changes in women. J. Lipid Res. 51(3), 625–634 (2010).
  • Romaine SP, Bailey KM, Hall AS, Balmforth AJ. The influence of SLCO1B1 (OATP1B1) gene polymorphisms on response to statin therapy. Pharmacogenomics J. 10(1), 1–11 (2010).
  • Hedman M, Antikainen M, Holmberg C et al. Pharmacokinetics and response to pravastatin in paediatric patients with familial hypercholesterolaemia and in paediatric cardiac transplant recipients in relation to polymorphisms of the SLCO1B1 and ABCB1 genes. Br. J. Clin. Pharmacol. 61(6), 706–715 (2006).
  • Martin NG, Li KW, Murray H, Putt W, Packard CJ, Humphries SE. The effects of a single nucleotide polymorphism in SLCO1B1 on the pharmacodynamics of pravastatin. Br. J. Clin. Pharmacol. 73(2), 303–306 (2012).
  • Yang GP, Yuan H, Tang B et al. Lack of effect of genetic polymorphisms of SLCO1B1 on the lipid-lowering response to pitavastatin in Chinese patients. Acta Pharmacol. Sin. 31(3), 382–386 (2010).
  • Winkelmann BR, Hoffmann MM, Nauck M et al. Haplotypes of the cholesteryl ester transfer protein gene predict lipid-modifying response to statin therapy. Pharmacogenomics J. 3(5), 284–296 (2003).
  • Bercovich D, Friedlander Y, Korem S et al. The association of common SNPs and haplotypes in the CETP and MDR1 genes with lipids response to fluvastatin in familial hypercholesterolemia. Atherosclerosis 185(1), 97–107 (2006).
  • Anagnostopoulou K, Kolovou G, Kostakou P, Mihas C, Mikhailidis D, Cokkinos DV. Pharmacogenetic study of cholesteryl ester transfer protein gene and simvastatin treatment in hypercholesterolaemic subjects. Expert Opin. Pharmacother. 8(15), 2459–2463 (2007).
  • Boekholdt SM, Sacks FM, Jukema JW et al. Cholesteryl ester transfer protein TaqIB variant, high-density lipoprotein cholesterol levels, cardiovascular risk, and efficacy of pravastatin treatment: individual patient meta-analysis of 13,677 subjects. Circulation 111(3), 278–287 (2005).
  • Redondo S, Martínez-González J, Urraca C, Tejerina T. Emerging therapeutic strategies to enhance HDL function. Lipids Health Dis. 10, 175 (2011).
  • Barter PJ, Rye KA. Cholesteryl ester transfer protein (CETP) inhibition as a strategy to reduce cardiovascular risk. J. Lipid Res. 53(9), 1755–1766 (2012).
  • AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N. Engl. J. Med. 365(24), 2255–2267 (2011).
  • Michos ED, Sibley CT, Baer JT, Blaha MJ, Blumenthal RS. Niacin and statin combination therapy for atherosclerosis regression and prevention of cardiovascular disease events: reconciling the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Sow HDL/High Triglycerides: Impact on Global Health Outcomes) trial with previous surrogate end point trials. J. Am. Coll. Cardiol. 59(23), 2058–2064 (2012).
  • Hansen MK, McVey MJ, White RF et al. Selective CETP inhibition and PPARalpha agonism increase HDL cholesterol and reduce LDL cholesterol in human ApoB100/human CETP transgenic mice. J. Cardiovasc. Pharmacol. Ther. 15(2), 196–202 (2010).
  • Yvan-Charvet L, Kling J, Pagler T et al. Cholesterol efflux potential and anti-inflammatory properties of high-density lipoprotein after treatment with niacin or anacetrapib. Arterioscler. Thromb. Vasc. Biol. 30(7), 1430–1438 (2010).
  • Degoma EM, Rader DJ. Novel HDL-directed pharmacotherapeutic strategies. Nat. Rev. Cardiol. 8(5), 266–277 (2011).
  • NCI-NHGRI Working Group on Replication in Association Studies. Replicating genotype–phenotype associations. Nature 447(7145), 655–660 (2007).
  • Ioannidis JP, Ntzani EE, Trikalinos TA, Contopoulos-Ioannidis DG. Replication validity of genetic association studies. Nat. Genet. 29(3), 306–309 (2001).
  • Daly AK. Genome-wide association studies in pharmacogenomics. Nat. Rev. Genet. 11(4), 241–246 (2010).
  • Couillard C, Després JP, Lamarche B et al. Effects of endurance exercise training on plasma HDL cholesterol levels depend on levels of triglycerides: evidence from men of the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) family Study. Arterioscler. Thromb. Vasc. Biol. 21(7), 1226–1232 (2001).
  • Siri-Tarino PW. Effects of diet on high-density lipoprotein cholesterol. Curr. Atheroscler. Rep. 13(6), 453–460 (2011).
  • Northwood EL, Elliott F, Forman D et al. Polymorphisms in xenobiotic metabolizing enzymes and diet influence colorectal adenoma risk. Pharmacogenet. Genomics 20(5), 315–326 (2010).
  • Kitzmiller JP, Groen DK, Phelps MA, Sadee W. Pharmacogenomic testing: relevance in medical practice: why drugs work in some patients but not in others. Cleve. Clin. J. Med. 78(4), 243–257 (2011).
  • Woodcock J. Assessing the clinical utility of diagnostics used in drug therapy. Clin. Pharmacol. Ther. 88(6), 765–773 (2010).
  • Tzvetkov M, von Ahsen N. Pharmacogenetic screening for drug therapy: from single gene markers to decision making in the next generation sequencing era. Pathology 44(2), 166–180 (2012).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.