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Review

Atherosclerosis regression and high-density lipoproteins

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Pages 1325-1334 | Published online: 10 Jan 2014

References

  • Ross R. Atherosclerosis – an inflammatory disease. N. Engl. J. Med.340, 115–126 (1999).
  • Small DM, Bond MG, Waugh D et al. Physicochemical and histological changes in the arterial wall of nonhuman primates during progression and regression of atherosclerosis. J. Clin. Invest.73, 1590–1605 (1984).
  • Badimon J, Badimon L, Fuster V. Regression of atherosclerotic lesions by high density lipoprotein plasma fraction in the cholesterol-fed rabbit. J. Clin. Invest.85, 1234–1241 (1990).
  • Plump AS, Smith JD, Hayek T et al. Severe hypercholesterolemia and atherosclerosis in Apolipoprotein E-deficient mice created by homologous recombination in ES cells. Cell 71, 343–353 (1992).
  • Kashyap VS, Santamarina-Fojo S, Brown DR et al. Apolipoprotein E deficiency in mice: gene replacement and prevention of atherosclerosis using adenovirus vectors. J. Clin. Invest.96, 1612–1620 (1995).
  • Reis ED, Li J, Fayad ZA et al. Dramatic remodeling of advanced atherosclerotic plaques of the Apolipoprotein E-deficient mouse in a novel transplantation model. J. Vasc. Surg.34, 541–547 (2001).
  • Grundy SM, Cleeman JI, Merz CNB et al. Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. Arterioscler. Thromb. Vasc. Biol.24, e149–e161 (2004).
  • MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20536 high-risk individuals: a randomised placebo-controlled trial. Lancet360, 7–22 (2002).
  • Gordon T, Castelli WP, Hjortland MC et al. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am. J. Med.62, 707–714 (1977).
  • Gordon DJ, Probstfield JL, Garrison RJ et al. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation79, 8–15 (1989).
  • Assmann G, Schulte H. Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM Experience). Prospective Cardiovascular Munster study. Am. J. Cardiol.70, 733–737 (1992).
  • Grundy SM, Cleeman JI, Daniels SR et al. diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement: Executive Summary. Circulation112, e285–e290 (2005).
  • Dekker JM, Girman C, Rhodes T et al. Metabolic syndrome and 10-year cardiovascular disease risk in the Hoorn Study. Circulation112, 666–673 (2005).
  • Haffner SM, Lehto S, Ronnemaa T et al. Mortality from coronary heart disease in subjects with Type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N. Engl. J. Med.339, 229 (1998).
  • Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic. Nature414, 782–787 (2001).
  • Bruckert E, Baccara-Dinet M, McCoy F et al. High prevalence of low HDL-cholesterol in a pan-European survey of 8545 dyslipidaemic patients. Curr. Med. Res. Opin.21, 1927–1934 (2005).
  • Nichols GA, Ambegaonkar BM, Sazonov V et al. Frequency of obtaining National Cholesterol Education Program Adult Treatment Panel III goals for all major serum lipoproteins after initiation of lipid altering therapy. Am. J. Cardiol.104, 1689–1694 (2009).
  • Grover SA, Kaouache M, Joseph L et al. Evaluating the incremental benefits of raising high-density lipoprotein cholesterol levels during lipid therapy after adjustment for the reductions in other blood lipid levels. Arch. Intern. Med.169, 1775–1780 (2009).
  • Miyazaki A, Rahim ATMA, Ohta T et al. High density lipoprotein mediates selective reduction in cholesteryl esters from macrophage foam cells. Biochim. Biophys. Acta1126, 73 (1992).
  • Oram JF, Lawn RM. ABCA1. The gatekeeper for eliminating excess tissue cholesterol. J. Lipid. Res.42, 1173–1179 (2001).
  • Gelissen IC, Harris M, Rye K-A et al. ABCA1 and ABCG1 synergize to mediate cholesterol export to ApoA-I. Arterioscler. Thromb. Vasc. Biol.26(3), 534–540 (2005).
  • Rubin EM, Krauss RM, Spangler EA et al. Inhibition of early atherogenesis in transgenic mice by human apolipoprotein AI. Nature353, 265–267 (1991).
  • Rong JX, Li J, Reis ED et al. Elevating high-density lipoprotein cholesterol in Apolipoprotein E-deficient mice remodels advanced atherosclerotic lesions by decreasing macrophage and increasing smooth muscle cell content. Circulation104, 2447–2452 (2001).
  • Choudhury RP, Rong JX, Trogan E et al. High-density lipoproteins retard the progression of atherosclerosis and favorably remodel lesions without suppressing indices of inflammation or oxidation. Arterioscler. Thromb. Vasc. Biol.24, 1904–1909 (2004).
  • Llodra J, Angeli V, Liu J et al. Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques. Proc. Natl Acad. Sci. USA101, 11779–11784 (2004).
  • Trogan E, Feig JE, Dogan S et al. Gene expression changes in foam cells and the role of chemokine receptor CCR7 during atherosclerosis regression in ApoE-deficient mice. Proc. Natl Acad. Sci. USA103, 3781–3786 (2006).
  • Cockerill GW, Rye KA, Gamble JR et al. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler. Thromb. Vasc. Biol.15, 1987–1994 (1995).
  • Nicholls SJ, Cutri B, Worthley SG et al. Impact of short-term administration of high-density lipoproteins and atorvastatin on atherosclerosis in rabbits. Arterioscler. Thromb. Vasc. Biol.25, 2416–2421 (2005).
  • Nicholls SJ, Dusting GJ, Cutri B et al. Reconstituted high-density lipoproteins inhibit the acute pro-oxidant and proinflammatory vascular changes induced by a periarterial collar in normocholesterolemic rabbits. Circulation111, 1543–1550 (2005).
  • Fogelman AM, Shechter I, Seager J et al. Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages. Proc. Natl Acad. Sci. USA77, 2214–2218 (1980).
  • Watson AD, Berliner JA, Hama SY et al. Protective effect of high density lipoprotein associated paraoxonase. Inhibition of the biological activity of minimally oxidized low density lipoprotein. J. Clin. Invest.96, 2882–2891 (1995).
  • Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett.286, 152 (1991).
  • Garner B, Waldeck AR, Witting PK et al. Oxidation of High Density Lipoproteins. II. Evidence for direct reduction of lipid hydroperoxides by methionine residues of Apolipoprotetins AI and AII. J. Biol. Chem.273, 6088–6095 (1998).
  • Glagov S, Weisenberg E, Zarins CK et al. Compensatory enlargement of human atherosclerotic coronary arteries. N. Engl. J. Med.316, 1371–1375 (1987).
  • Blankenhorn DH, Nessim SA, Johnson RL et al. Beneficial effects of combined colestipol–niacin therapy on coronary atherosclerosis and coronary venous bypass grafts. JAMA257, 3233–3240 (1987).
  • Cashin-Hemphill L, Mack WJ, Pogoda JM et al. Beneficial effects of colestipol-niacin on coronary atherosclerosis. A 4-year follow-up. JAMA264, 3013–3017 (1990).
  • Brown G, Albers JJ, Fisher LD et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N. Engl. J. Med.323, 1289–1298 (1990).
  • Brown BG, Zhao X-Q, Chait A et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N. Engl. J. Med.345, 1583–1592 (2001).
  • Whitney EJ, Krasuski RA, Personius BE et al. A randomized trial of a strategy for increasing high-density lipoprotein cholesterol levels: effects on progression of coronary heart disease and clinical events. Ann. Intern. Med.142, 95–104 (2005).
  • Topol EJ, Nissen SE. Our preoccupation with coronary luminology. The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation92, 2333–2342 (1995).
  • Bots ML, Evans GW, Riley WA et al. Carotid intima–media thickness measurements in intervention studies: design options, progression rates, and sample size considerations: a point of view. Stroke34, 2985–2994 (2003).
  • Nissen SE, Tsunoda T, Tuzcu EM et al. Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial. JAMA290, 2292–2300 (2003).
  • Nissen SE, Tardif JC, Nicholls SJ et al. Effect of torcetrapib on the progression of coronary atherosclerosis. N. Engl. J. Med.356, 1304–1316 (2007).
  • Nissen SE, Nicholls SJ, Wolski K et al. Comparison of pioglitazone vs glimepiride on progression of coronary atherosclerosis in patients with Type 2 diabetes: the PERISCOPE randomized controlled trial. JAMA299, 1561–1573 (2008).
  • Corti R, Fayad ZA, Fuster V et al. Effects of lipid-lowering by simvastatin on human atherosclerotic lesions: a longitudinal study by high-resolution, noninvasive magnetic resonance imaging. Circulation104, 249–252 (2001).
  • Lee JM, Wiesmann F, Shirodaria C et al. Early changes in arterial structure and function following statin initiation: quantification by magnetic resonance imaging. Atherosclerosis197, 951–958 (2008).
  • Saam T, Kerwin WS, Chu B et al. Sample size calculation for clinical trials using magnetic resonance imaging for the quantitative assessment of carotid atherosclerosis. J. Cardiovasc. Magn. Reson.7, 799–808 (2005).
  • Varghese A, Crowe LA, Mohiaddin RH et al. Interstudy reproducibility of three-dimensional volume-selective fast spin echo magnetic resonance for quantifying carotid artery wall volume. J. Magn. Reson. Imag.21, 187–191 (2005).
  • Duivenvoorden R, de Groot E, Elsen BM et al.In vivo quantification of carotid artery wall dimensions: 3.0-Tesla MRI versus B-mode ultrasound imaging. Circ. Cardiovasc. Imag.2, 235–242 (2009).
  • Yuan C, Mitsumori LM, Beach KW et al. Carotid atherosclerotic plaque: noninvasive MR characterization and identification of vulnerable lesions. Radiology221, 285–299 (2001).
  • Saam T, Ferguson MS, Yarnykh VL et al. Quantitative evaluation of carotid plaque composition by in vivo MRI. Arterioscler. Thromb. Vasc. Biol.25, 234–239 (2005).
  • Zhao X-Q, Yuan C, Hatsukami TS et al. Effects of prolonged intensive lipid-lowering therapy on the characteristics of carotid atherosclerotic plaques in vivo by MRI: a case–control study. Arterioscler. Thromb. Vasc. Biol.21, 1623–1629 (2001).
  • Underhill HR, Yuan C, Zhao XQ et al. Effect of rosuvastatin therapy on carotid plaque morphology and composition in moderately hypercholesterolemic patients: a high-resolution magnetic resonance imaging trial. Am. Heart J.155, 584.e1–8 (2008).
  • Prati F, Regar E, Mintz GS et al. Expert review document on methodology, terminology, and clinical applications of optical coherence tomography: physical principles, methodology of image acquisition, and clinical application for assessment of coronary arteries and atherosclerosis. Eur. Heart J.31, 401–415 (2009).
  • Rudd JH, Myers KS, Bansilal S et al.18Fluorodeoxyglucose positron emission tomography imaging of atherosclerotic plaque inflammation is highly reproducible: implications for atherosclerosis therapy trials. J. Am. Coll. Cardiol.50, 892–896 (2007).
  • No authors listed. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet344, 1383–1389 (1994).
  • Baigent C, Keech A, Kearney PM et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet366, 1267–1278 (2005).
  • Wierzbicki AS, Mikhailidis DP. Dose-response effects of atorvastatin and simvastatin on high-density lipoprotein cholesterol in hypercholesterolaemic patients: a review of five comparative studies. Int. J. Cardiol.84, 53–57 (2002).
  • Taylor AJ, Kent SM, Flaherty PJ et al. ARBITER: Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol: a randomized trial comparing the effects of atorvastatin and pravastatin on carotid intima medial thickness. Circulation106, 2055–2060 (2002).
  • de Groot E, Jukema JW, Montauban van Swijndregt AD et al. B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). J. Am. Coll. Cardiol.31, 1561–1567 (1998).
  • Nissen SE, Tuzcu EM, Schoenhagen P et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N. Engl. J. Med.352, 29–38 (2005).
  • Nissen SE, Nicholls SJ, Sipahi I et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA295, 1556–1565 (2006).
  • Nicholls SJ, Tuzcu EM, Sipahi I et al. Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis. JAMA297, 499–508 (2007).
  • Altschul R, Hoffer A, Stephen JD. Influence of nicotinic acid on serum cholesterol in man. Arch. Biochem.54, 558–559 (1955).
  • Morgan JM, Capuzzi DM, Guyton JR et al. Treatment effect of Niaspan, a controlled-release niacin, in patients with hypercholesterolemia: a placebo-controlled trial. J. Cardiovasc. Pharmacol. Ther.1, 195–202 (1996).
  • Morgan J, Capuzzi D, Guyton J. A new extended-release niacin (Niaspan): efficacy, tolerability, and safety in hypercholesterolemic patients. Am. J. Cardiol.82, 29U–34U (1998).
  • Tunaru S, Kero J, Schaub A et al. PUMA-G and HM74 are receptors for nicotinic acid and mediate its anti-lipolytic effect. Nat. Med.9, 352–355 (2003).
  • van der Hoorn JW, de Haan W, Berbee 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, 2016–2022 (2008).
  • Ganji SH, Tavintharan S, Zhu D et al. Niacin noncompetitively inhibits DGAT2 but not DGAT1 activity in HepG2 cells. J. Lipid. Res.45, 1835–1845 (2004).
  • Jin FY, Kamanna VS, Kashyap ML. Niacin accelerates intracellular ApoB degradation by inhibiting triacylglycerol synthesis in human hepatoblastoma (HepG2) cells. Arterioscler. Thromb. Vasc. Biol.19, 1051–1059 (1999).
  • Shepherd J, Packard CJ, Patsch JR et al. Effects of nicotinic acid therapy on plasma high density lipoprotein subfraction distribution and composition and on Apolipoprotein A metabolism. J. Clin. Invest.63, 858–867 (1979).
  • Jin F-Y, Kamanna VS, Kashyap ML. Niacin decreases removal of high-density lipoprotein apolipoprotein A-I but not cholesterol ester by Hep G2 cells: implication for reverse cholesterol transport. Arterioscler. Thromb. Vasc. Biol.17, 2020–2028 (1997).
  • Martinez LO, Jacquet S, Esteve JP et al. Ectopic β-chain of ATP synthase is an apolipoprotein A-I receptor in hepatic HDL endocytosis. Nature421, 75–79 (2003).
  • Zhang LH, Kamanna VS, Zhang MC et al. Niacin inhibits surface expression of ATP synthase β chain in HepG2 cells: implications for raising HDL. J. Lipid. Res.49, 1195–1201 (2008).
  • Rubic T, Trottmann M, Lorenz RL. Stimulation of CD36 and the key effector of reverse cholesterol transport ATP-binding cassette A1 in monocytoid cells by niacin. Biochem. Pharmacol.67, 411–419 (2004).
  • Knowles HJ, te Poele RH, Workman P et al. Niacin induces PPARγ expression and transcriptional activation in macrophages via HM74 and HM74a-mediated induction of prostaglandin synthesis pathways. Biochem. Pharmacol.71, 646–656 (2006).
  • Taylor AJ, Sullenberger LE, Lee HJ et al. Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2: a double-blind, placebo-controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins. Circulation110, 3512–3517 (2004).
  • Lee JM, Robson MD, Yu LM et al. Effects of high-dose modified-release nicotinic acid on atherosclerosis and vascular function: a randomized, placebo-controlled, magnetic resonance imaging study. J. Am. Coll. Cardiol.54, 1787–1794 (2009).
  • Taylor AJ, Villines TC, Stanek EJ et al. Extended-release niacin or ezetimibe and carotid intima–media thickness. N. Engl. J. Med.361, 2113–2122 (2009).
  • Canner PL, Berge KG, Wenger NK et al. Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J. Am. Coll. Cardiol.8, 1245–1255 (1986).
  • Rubins HB, Robins SJ, Collins D et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. N. Engl. J. Med.341, 410–418 (1999).
  • No authors listed. Secondary Prevention by raising HDL Cholesterol and reducing triglycerides in patients with coronary artery disease: the Bezafibrate Infarction Prevention (BIP) Study. Circulation102, 21–27 (2000).
  • Keech A, Simes RJ, Barter P et al.; FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with Type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet366, 1849 (2005).
  • Ginsberg HN, Elam MB, Lovato LC et al. Effects of combination lipid therapy in Type 2 diabetes mellitus. N. Engl. J. Med.362, 1563–1574 (2010).
  • Hiukka A, Westerbacka J, Leinonen ES et al. Long-term effects of fenofibrate on carotid intima–media thickness and augmentation index in subjects with Type 2 diabetes mellitus. J. Am. Coll. Cardiol.52, 2190–2197 (2008).
  • Ayaori M, Momiyama Y, Fayad ZA et al. Effect of bezafibrate therapy on atherosclerotic aortic plaques detected by MRI in dyslipidemic patients with hypertriglyceridemia. Atherosclerosis196, 425–433 (2008).
  • Dormandy JA, Charbonnel B, Eckland DJ et al. Secondary prevention of macrovascular events in patients with Type 2 diabetes in the PROactive Study (Prospective Pioglitazone Clinical Trial in Macrovascular Events): a randomised controlled trial. Lancet366, 1279 (2005).
  • Freed MI, Ratner R, Marcovina SM et al. Effects of rosiglitazone alone and in combination with atorvastatin on the metabolic abnormalities in Type 2 diabetes mellitus. Am. J. Cardiol.90, 947 (2002).
  • Goldberg RB, Kendall DM, Deeg MA et al. A Comparison of lipid and glycemic effects of pioglitazone and rosiglitazone in patients with Type 2 diabetes and dyslipidemia. Diabetes Care28, 1547–1554 (2005).
  • Sidhu JS, Kaposzta Z, Markus HS et al. Effect of rosiglitazone on common carotid intima–media thickness progression in coronary artery disease patients without diabetes mellitus. Arterioscler. Thromb. Vasc. Biol.24, 930–934 (2004).
  • Varghese A, Yee MS, Chan CF et al. Effect of rosiglitazone on progression of atherosclerosis: insights using 3D carotid cardiovascular magnetic resonance. J. Cardiovasc. Magn. Reson.11, 24 (2009).
  • Brousseau ME, Schaefer EJ, Wolfe ML et al. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N. Engl. J. Med.350, 1505–1515 (2004).
  • Okamoto H, Yonemori F, Wakitani K et al. A cholesteryl ester transfer protein inhibitor attenuates atherosclerosis in rabbits. Nature406, 203–207 (2000).
  • Ordovas JM, Cupples LA, Corella D et al. Association of cholesteryl ester transfer protein-TaqIB polymorphism with variations in lipoprotein subclasses and coronary heart disease risk: the Framingham study. Arterioscler. Thromb. Vasc. Biol.20, 1323–1329 (2000).
  • Thompson A, Di Angelantonio E, Sarwar N et al. Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk. JAMA299, 2777–2788 (2008).
  • Zhong S, Sharp DS, Grove JS et al. Increased coronary heart disease in japanese-american men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels. J. Clin. Invest.97, 2917–2923 (1996).
  • Duwensee K, Breitling LP, Tancevski I et al. Cholesteryl ester transfer protein in patients with coronary heart disease. Eur. J. Clin. Invest.40(7), 616–622 (2010).
  • Barter PJ, Caulfield M, Eriksson M et al. Effects of torcetrapib in patients at high risk for coronary events. N. Engl. J. Med.357, 2109–2122 (2007).
  • Bots ML, Visseren FL, Evans GW et al. Torcetrapib and carotid intima–media thickness in mixed dyslipidaemia (RADIANCE 2 study): a randomised, double-blind trial. Lancet370, 153–160 (2007).
  • Kastelein JJ, van Leuven SI, Burgess L et al. Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N. Engl. J. Med.356, 1620–1630 (2007).
  • Schwartz GG, Olsson AG, Ballantyne CM et al. Rationale and design of the dal-OUTCOMES trial: efficacy and safety of dalcetrapib in patients with recent acute coronary syndrome. Am. Heart J.158, 896–901.e3 (2009).
  • Stein EA, Stroes ES, Steiner G et al. Safety and tolerability of dalcetrapib. Am. J. Cardiol.104, 82–91 (2009).
  • Ranalletta M, Bierilo KK, Chen Y et al. Biochemical characterization of cholesteryl ester transfer protein inhibitors. J. Lipid Res.51, 2739–2752 (2010).
  • Robinson JG. Dalcetrapib: a review of Phase II data. Expert Opin. Invest. Drugs19, 795–805 (2010).
  • Franceschini G, Sirtori CR, Capurso A 2nd et al. A-IMilano apoprotein. Decreased high density lipoprotein cholesterol levels with significant lipoprotein modifications and without clinical atherosclerosis in an Italian family. J. Clin. Invest.66, 892–900 (1980).
  • Franceschini G, Calabresi L, Chiesa G et al. Increased cholesterol efflux potential of sera from ApoA-IMilano carriers and transgenic mice. Arterioscler. Thromb. Vasc. Biol.19, 1257–1262 (1999).
  • Shah PK, Yano J, Reyes O et al. High-dose recombinant Apolipoprotein A-IMilano mobilizes tissue cholesterol and rapidly reduces plaque lipid and macrophage content in Apolipoprotein E-deficient mice: potential implications for acute plaque stabilization. Circulation103, 3047–3050 (2001).
  • Ibanez B, Vilahur G, Cimmino G et al. Rapid change in plaque size, composition, and molecular footprint after recombinant apolipoprotein A-I Milano (ETC-216) administration: magnetic resonance imaging study in an experimental model of atherosclerosis. J. Am. Coll. Cardiol.51, 1104–1109 (2008).
  • Navab M, Anantharamaiah GM, Reddy ST et al. Apolipoprotein A-I mimetic peptides. Arterioscler. Thromb. Vasc. Biol.25, 1325–1331 (2005).
  • Navab M, Anantharamaiah GM, Hama S et al. Oral administration of an Apo A-I mimetic peptide synthesized from D-amino acids dramatically reduces atherosclerosis in mice independent of plasma cholesterol. Circulation105, 290–292 (2002).
  • Zheng L, Nukuna B, Brennan M-L et al. Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease. J. Clin. Invest.114, 529–541 (2004).
  • Hansel B, Giral P, Nobecourt E et al. metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity. J. Clin. Endocrinol. Metab.89, 4963–4971 (2004).
  • Navab M, Reddy ST, Van Lenten BJ et al. The role of dysfunctional HDL in atherosclerosis. J. Lipid. Res.50(Suppl.), S145–S149 (2009).
  • de la Llera Moya M, Atger V, Paul JL et al. A cell culture system for screening human serum for ability to promote cellular cholesterol efflux. Relations between serum components and efflux, esterification, and transfer. Arterioscler. Thromb.14, 1056–1065 (1994).
  • Zhang Y, Zanotti I, Reilly MP et al. Overexpression of Apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation108, 661–663 (2003).
  • Navab M, Hama SY, Hough GP et al. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J. Lipid. Res.42, 1308–1317 (2001).
  • Ansell BJ, Navab M, Hama S et al. Inflammatory/antiinflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment. Circulation108, 2751–2756 (2003).
  • Navab M, Anantharamaiah GM, Reddy ST et al. Mechanisms of disease: proatherogenic HDL – an evolving field. Nat. Clin. Pract. Endocrinol. Metab.2, 504–511 (2006).

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