Update on strategies to increase HDL quantity and function (original) (raw)

• Boden, W. E. High-density lipoprotein cholesterol as an independent risk factor in cardiovascular disease: assessing the data from Framingham to the Veterans Affairs High-density lipoprotein intervention trial. Am. J. Cardiol. 86, 19L–22L (2000).
  CAS PubMed Google Scholar
• Barter, P. et al. HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. N. Engl. J. Med. 357, 1301–1310 (2007).
  CAS PubMed Google Scholar
• Lewis, G. F. & Rader, D. J. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circ. Res. 96, 1221–1232 (2005).
  CAS PubMed Google Scholar
• Cuchel, M. & Rader, D. J. Macrophage reverse cholesterol transport: key to the regression of atherosclerosis? Circulation 113, 2548–2555 (2006).
  PubMed Google Scholar
• Rader, D. J. Molecular regulation of HDL metabolism and function: implications for novel therapies. J. Clin. Invest. 116, 3090–3100 (2006).
  CAS PubMed PubMed Central Google Scholar
• Florentin, M., Liberopoulos, E. N., Wierzbicki, A. S. & Mikhailidis, D. P. Multiple actions of high-density lipoprotein. Curr. Opin. Cardiol. 23, 370–378 (2008).
  PubMed Google Scholar
• Chiesa, G. & Sirtori, C. R. Apolipoprotein A-I Milano: current perspectives. Curr. Opin. Lipidol. 14, 159–163 (2003).
  CAS PubMed Google Scholar
• Nissen, S. E. et al. Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial. JAMA 290, 2292–2300 (2003).
  CAS PubMed Google Scholar
• Zhang, Y. et al. Hepatic expression of scavenger receptor class B type I (SR-BI) is a positive regulator of macrophage reverse cholesterol transport in vivo. J. Clin. Invest. 115, 2870–2874 (2005).
  CAS PubMed PubMed Central Google Scholar
• Barter, P. J. et al. Effects of torcetrapib in patients at high risk for coronary events. N. Engl. J. Med. 357, 2109–2122 (2007).
  CAS PubMed Google Scholar
• Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 285, 2486–2497 (2001).
• Carlson, L. A. Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J. Intern. Med. 258, 94–114 (2005).
  CAS PubMed Google Scholar
• The coronary drug project research group. Clofibrate and niacin in coronary heart disease. JAMA 231, 360–381 (1975).
• Brown, B. G. et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N. Engl. J. Med. 345, 1583–1592 (2001).
  CAS PubMed Google Scholar
• Taylor, A. J., Sullenberger, L. E., Lee, H. J., Lee, J. K. & Grace, K. A. 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. Circulation 110, 3512–3517 (2004).
  CAS PubMed Google Scholar
• AIM HIGH: Niacin Plus Statin to Prevent Vascular Events. ClincialTrials.gov [online], (2009).
• A Randomized Trial of the Long-term Clinical Effects of Raising HDL Cholesterol With Extended Release Niacin/Laropiprant ClinicalTrials.gov [online], (2007).
• Tunaru, S. et al. PUMA-G and HM74 are receptors for nicotinic acid and mediate its anti-lipolytic effect. Nat.Med. 9, 352–355 (2003).
  CAS PubMed Google Scholar
• Soga, T. et al. Molecular identification of nicotinic acid receptor. Biochem. Biophys. Res. Commun. 303, 364–369 (2003).
  CAS PubMed Google Scholar
• Wise, A. et al. Molecular identification of high and low affinity receptors for nicotinic acid. J. Biol. Chem. 278, 9869–9874 (2003).
  CAS PubMed Google Scholar
• Zhang, Y. et al. Niacin mediates lipolysis in adipose tissue through its G-protein coupled receptor HM74A. Biochem. Biophys. Res. Commun. 334, 729–732 (2005).
  CAS PubMed Google Scholar
• Ganji, S. H. et al. Niacin noncompetitively inhibits DGAT2 but not DGAT1 activity in HepG2 cells. J. Lipid Res. 45, 1835–1845 (2004).
  CAS PubMed Google Scholar
• Zhang, L. H., Kamanna, V. S., Zhang, M. C. & Kashyap, M. L. Niacin inhibits surface expression of ATP synthase β chain in HepG2 cells: implications for raising HDL. J. Lipid Res. 49, 1195–1201 (2008).
  CAS PubMed Google Scholar
• Martinez, L. O. et al. Ectopic β-chain of ATP synthase is an apolipoprotein A-I receptor in hepatic HDL endocytosis. Nature 421, 75–79 (2003).
  CAS PubMed Google Scholar
• van der Hoorn, J. W. 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).
  CAS PubMed Google Scholar
• Cefali, E. A., Simmons, P. D., Stanek, E. J. & Shamp, T. R. Improved control of niacin-induced flushing using an optimized once-daily, extended-release niacin formulation. Int. J. Clin. Pharmacol. Ther. 44, 633–640 (2006).
  CAS PubMed Google Scholar
• Benyo, Z. et al. GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. J. Clin. Invest. 115, 3634–3640 (2005).
  CAS PubMed PubMed Central Google Scholar
• Cheng, K. et al. Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. Proc. Natl Acad. Sci. USA 103, 6682–6687 (2006).
  CAS PubMed PubMed Central Google Scholar
• Lai, E. et al. Suppression of niacin-induced vasodilation with an antagonist to prostaglandin D2 receptor subtype 1. Clin. Pharmacol. Ther. 81, 849–857 (2007).
  CAS PubMed Google Scholar
• Paolini, J. F. et al. Effects of laropiprant on nicotinic acid-induced flushing in patients with dyslipidemia. Am. J. Cardiol. 101, 625–630 (2008).
  CAS PubMed Google Scholar
• Walters, R. W. et al. β-Arrestin1 mediates nicotinic acid-induced flushing, but not its antilipolytic effect, in mice. J. Clin. Invest. doi: 10.1172/JCI36806.
  CAS Google Scholar
• Clark, R. W. et al. Raising high-density lipoprotein in humans through inhibition of cholesteryl ester transfer protein: an initial multidose study of torcetrapib. Arterioscler. Thromb. Vasc. Biol. 24, 490–497 (2004).
  CAS PubMed Google Scholar
• Brousseau, M. E. et al. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N. Engl. J. Med. 350, 1505–1515 (2004).
  CAS PubMed Google Scholar
• Brown, M. L. et al. Molecular basis of lipid transfer protein deficiency in a family with increased high-density lipoproteins. Nature 342, 448–451 (1989).
  CAS PubMed Google Scholar
• Inazu, A. et al. Increased high-density lipoprotein levels caused by a common cholesteryl-ester transfer protein gene mutation. N. Engl. J. Med. 323, 1234–1238 (1990).
  CAS PubMed Google Scholar
• Nissen, S. E. et al. Effect of torcetrapib on the progression of coronary atherosclerosis. N. Engl. J. Med. 356, 1304–1316 (2007).
  CAS PubMed Google Scholar
• Kastelein, J. J. P. et al. Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N. Engl. J. Med. 356, 1620–1630 (2007).
  CAS PubMed Google Scholar
• Matsuura, F., Wang, N., Chen, W., Jiang, X. C. & Tall, A. R. HDL from CETP-deficient subjects shows enhanced ability to promote cholesterol efflux from macrophages in an apoE- and ABCG1-dependent pathway. J. Clin. Invest. 116, 1435–1442 (2006).
  CAS PubMed PubMed Central Google Scholar
• Yvan-Charvet, L. et al. Inhibition of cholesteryl ester transfer protein by torcetrapib modestly increases macrophage cholesterol efflux to HDL. Arterioscler. Thromb. Vasc. Biol. 27, 1132–1138 (2007).
  CAS PubMed Google Scholar
• Krishna, R. et al. Effect of the cholesteryl ester transfer protein inhibitor, anacetrapib, on lipoproteins in patients with dyslipidaemia and on 24-h ambulatory blood pressure in healthy individuals: two double-blind, randomised placebo-controlled phase I studies. Lancet 370, 1907–1914 (2007).
  CAS PubMed Google Scholar
• Bloomfield, D. et al. Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib as monotherapy and co-administered with atorvastatin in dyslipidemic patients. Am. Heart J. 157, 352–360 e2 (2009).
  CAS PubMed Google Scholar
• A 76-Week, Worldwide, Multicenter, Double-Blind, Randomized, Placebo-Controlled Study to Assess the Tolerability and Efficacy of Anacetrapib When Added to Ongoing Therapy With a Statin in Patients with Coronary Heart Disease (CHD) or CHD Risk-Equivalent Disease. ClincialTrials.gov [online], (2009).
• de Grooth, G. J. et al. Efficacy and safety of a novel cholesteryl ester transfer protein inhibitor, JTT-705, in humans: a randomized phase II dose-response study. Circulation 105, 2159–2165 (2002).
  CAS PubMed Google Scholar
• Kuivenhoven, J. A. et al. Effectiveness of inhibition of cholesteryl ester transfer protein by JTT-705 in combination with pravastatin in type II dyslipidemia. Am. J. Cardiol. 95, 1085–1098 (2005).
  CAS PubMed Google Scholar
• A Randomized, Double-Blind, Placebo-Controlled Study Assessing the Effect of RO4607381 on Cardiovascular Mortality and Morbidity in Clinically Stable Patients With a Recent Acute Coronary Syndrome. ClinicalTrials.gov [online], (2008).
• Santamarina-Fojo, S., Lambert, G., Hoeg, J. M. & Brewer, H. B., Jr. Lecithin-cholesterol acyltransferase: role in lipoprotein metabolism, reverse cholesterol transport and atherosclerosis. Curr. Opin. Lipidol. 11, 267–275 (2000).
  CAS PubMed Google Scholar
• Hovingh, G. K. et al. Compromised LCAT function is associated with increased atherosclerosis. Circulation 112, 879–884 (2005).
  CAS PubMed Google Scholar
• Hoeg, J. M. et al. Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis. Proc. Natl Acad. Sci. USA 93, 11448–11453 (1996).
  CAS PubMed PubMed Central Google Scholar
• Foger, B. et al. Cholesteryl ester transfer protein corrects dysfunctional high density lipoproteins and reduces aortic atherosclerosis in lecithin cholesterol acyltransferase transgenic mice. J. Biol. Chem. 274, 36912–36920 (1999).
  CAS PubMed Google Scholar
• Mertens, A. et al. Increased low-density lipoprotein oxidation and impaired high-density lipoprotein antioxidant defense are associated with increased macrophage homing and atherosclerosis in dyslipidemic obese mice: LCAT gene transfer decreases atherosclerosis. Circulation 107, 1640–1646 (2003).
  CAS PubMed Google Scholar
• Esperion begins multiple-dose study of ETC-642 (RLT Peptide) in patients with stable atherosclerosis. [Online] (2003).
• Plump, A., Scott, C. & Breslow, J. Human apolipoprotein A-I gene expression increases high density lipoprotein and suppresses atherosclerosis in the apolipoprotein E-deficient mouse. Proc. Natl Acad. Sci. USA 91, 9607–9611 (1994).
  CAS PubMed PubMed Central Google Scholar
• Tangirala, R. K. et al. Regression of atherosclerosis induced by liver-directed gene transfer of apolipoprotein A-I in mice. Circulation 100, 1816–1822 (1999).
  CAS PubMed Google Scholar
• Zhang, Y. et al. Overexpression of apoA-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation 108, 661–663 (2003).
  CAS PubMed Google Scholar
• A Safety, Pharmacokinetic, and Pharmacodynamic Assessment of 28-Dy Oral Dosing of RVX000222 in Healthy Subjects and Subjects with Low High Density Lipoprotein (HDL). ClincialTrials.gov [online], (2008).
• Jaye, M. et al. A novel endothelial-derived lipase that modulates HDL metabolism. Nat. Genet. 21, 424–428 (1999).
  CAS PubMed Google Scholar
• Jin, W., Millar, J. S., Broedl, U., Glick, J. M. & Rader, D. J. Inhibition of endothelial lipase causes increased HDL cholesterol levels in vivo. J. Clin. Invest. 111, 357–362 (2003).
  CAS PubMed PubMed Central Google Scholar
• Badellino, K. O., Wolfe, M. L., Reilly, M. P. & Rader, D. J. Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis. PLoS Med. 3, e22 (2006).
  PubMed Google Scholar
• Badellino, K. O., Wolfe, M. L., Reilly, M. P. & Rader, D. J. Endothelial lipase is increased in vivo by inflammation in humans. Circulation 117, 678–685 (2008).
  CAS PubMed Google Scholar
• deLemos, A. S., Wolfe, M. L., Long, C. J., Sivapackianathan, R. & Rader, D. J. Identification of genetic variants in endothelial lipase in persons with elevated high-density lipoprotein cholesterol. Circulation 106, 1321–1326 (2002).
  CAS PubMed Google Scholar
• Tang, N. P. et al. Protective effect of an endothelial lipase gene variant on coronary artery disease in a Chinese population. J. Lipid Res. 49, 369–375 (2008).
  CAS PubMed Google Scholar
• Goodman, K. B. et al. Discovery of potent, selective sulfonylfuran urea endothelial lipase inhibitors. Bioorg. Med. Chem. Lett. 19, 27–30 (2009).
  CAS PubMed Google Scholar
• Li, A. C. & Glass, C. K. The macrophage foam cell as a target for therapeutic intervention. Nat. Med. 8, 1235–1242 (2002).
  CAS PubMed Google Scholar
• Wang, N., Lan, D., Chen, W., Matsuura, F. & Tall, A. R. ATP-binding cassette transporters G1 and G4 mediate cellular cholesterol efflux to high-density lipoproteins. Proc. Natl Acad. Sci. USA 101, 9774–9779 (2004).
  CAS PubMed PubMed Central Google Scholar
• Kennedy, M. A. et al. ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation. Cell Metab. 1, 121–131 (2005).
  CAS PubMed Google Scholar
• Hobbs, H. H. & Rader, D. J. ABC1: connecting yellow tonsils, neuropathy, and very low HDL. J. Clin. Invest. 104, 1015–1017 (1999).
  CAS PubMed PubMed Central Google Scholar
• Vaisman, B. L. et al. ABCA1 overexpression leads to hyperalphalipoproteinemia and increased biliary cholesterol excretion in transgenic mice. J. Clin. Invest. 108, 303–309 (2001).
  CAS PubMed PubMed Central Google Scholar
• Wang, X. et al. Macrophage ABCA1 and ABCG1, but not SR-BI, promote macrophage reverse cholesterol transport in vivo. J. Clin. Invest. 117, 2216–2224 (2007).
  CAS PubMed PubMed Central Google Scholar
• Repa, J. J. et al. Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers. Science 289, 1524–1529 (2000).
  CAS PubMed Google Scholar
• Terasaka, N. et al. T-0901317, a synthetic liver X receptor ligand, inhibits development of atherosclerosis in LDL receptor-deficient mice. FEBS Lett. 536, 6–11 (2003).
  CAS PubMed Google Scholar
• Naik, S. U. et al. Pharmacological activation of liver X receptors promotes reverse cholesterol transport in vivo. Circulation 113, 90–97 (2006).
  CAS PubMed Google Scholar
• Bultel, S. et al. Liver X receptor activation induces the uptake of cholesteryl esters from high density lipoprotein in primary human macrophages. Arterioscler. Thromb. Vasc. Biol. 28, 2288–2295 (2008).
  CAS PubMed Google Scholar
• Li, A. C. & Glass, C. K. PPAR- and LXR-dependent pathways controlling lipid metabolism and the development of atherosclerosis. J. Lipid Res. 45, 2161–2173 (2004).
  CAS PubMed Google Scholar
• Groot, P. H. E. et al. Synthetic LXR agonists increase LDL in CETP species. J. Lipid Res. 46, 2182–2191 (2005).
  CAS PubMed Google Scholar
• Molteni, V. et al. N-acylthiadiazolines, a new class of liver X receptor agonists with selectivity for LXRβ. J. Med. Chem. 50, 4255–4259 (2007).
  CAS PubMed Google Scholar
• [No authors listed] Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease: the Bezafibrate Infarction Prevention (BIP) study. Circulation 102, 21–27 (2000).
• Keech, A. et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 366, 1849–1861 (2005).
  CAS PubMed Google Scholar
• Chinetti, G. et al. PPARα and PPARγ activators induce cholesterol removal from human macrophage foam cells through stimulation of the ABCA1 pathway. Nat. Med. 7, 53–58 (2001).
  CAS PubMed Google Scholar
• Nissen, S. E. et al. Effects of a potent and selective PPARα agonist in patients with atherogenic dyslipidemia or hypercholesterolemia: two randomized controlled trials. JAMA 297, 1362–1373 (2007).
  CAS PubMed Google Scholar
• Millar, J. S. et al. Potent and selective PPARα agonist LY518674 upregulates both ApoA-I production and catabolism in human subjects with the metabolic syndrome. Arterioscler. Thromb. Vasc. Biol. 29, 140–146 (2009).
  CAS PubMed Google Scholar
• Nanjee, M. N. et al. Effects of intravenous infusion of lipid-free apo A-I in humans. Arterioscler. Thromb. Vasc. Biol. 16, 1203–1214 (1996).
  CAS PubMed Google Scholar
• Nanjee, M. N., Doran, J. E., Lerch, P. G. & Miller, N. E. Acute effects of intravenous infusion of ApoA1/phosphatidylcholine discs on plasma lipoproteins in humans. Arterioscler. Thromb. Vasc. Biol. 19, 979–989 (1999).
  CAS PubMed Google Scholar
• Nanjee, M. N. et al. Intravenous apoA-I/lecithin discs increase pre-β-HDL concentration in tissue fluid and stimulate reverse cholesterol transport in humans. J. Lipid Res. 42, 1586–1593 (2001).
  CAS PubMed Google Scholar
• Eriksson, M., Carlson, L. A., Miettinen, T. A. & Angelin, B. Stimulation of fecal steroid excretion after infusion of recombinant proapolipoprotein A-I: Potential reverse cholesterol transport in humans. Circulation 100, 594–598 (1999).
  CAS PubMed Google Scholar
• Tardif, J. C. et al. Effects of reconstituted high-density lipoprotein infusions on coronary atherosclerosis: a randomized controlled trial. JAMA 297, 1675–1682 (2007).
  PubMed Google Scholar
• Sacks, F. M. et al. Selective delipidation of plasma HDL enhances reverse cholesterol transport in vivo. J. Lipid Res. 50, 894–907 (2009).
  CAS PubMed PubMed Central Google Scholar
• Rader, D. J. High-density lipoproteins as an emerging therapeutic target for atherosclerosis. JAMA 290, 2322–2324 (2003).
  CAS PubMed Google Scholar
• Garber, D. W. et al. A new synthetic class A amphipathic peptide analogue protects mice from diet-induced atherosclerosis. J. Lipid Res. 42, 545–552 (2001).
  CAS PubMed Google Scholar
• Anantharamaiah, G. M. et al. Structural requirements for antioxidative and anti-inflammatory properties of apolipoprotein A-I-mimetic peptides. J. Lipid Res. 48, 1915–1923 (2007).
  CAS PubMed Google Scholar
• Navab, M. 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. Circulation 105, 290–292 (2002).
  CAS PubMed Google Scholar
• Navab, M. et al. Oral D-4F causes formation of pre-β high-density lipoprotein and improves high-density lipoprotein-mediated cholesterol efflux and reverse cholesterol transport from macrophages in apolipoprotein E-null mice. Circulation 109, 3215–3220 (2004).
  CAS PubMed Google Scholar
• Bloedon, L. T. et al. Safety, pharmacokinetics, and pharmacodynamics of oral apoA-I mimetic peptide D-4F in high-risk cardiovascular patients. J. Lipid Res. 49, 1344–1352 (2008).
  CAS PubMed PubMed Central Google Scholar