[1]
Linsel-Nitschke P, Tall AR. HDL as a target in the treatment of atherosclerotic cardiovascular disease. Nat Rev Drug Discov 2005; 4: 193-205.
DOI: 10.1038/nrd1658
Google Scholar
[2]
Spector R. Progress in the search for ideal drugs. Pharmacology 2002; 64(1): 1-7.
Google Scholar
[3]
Gotto AM Jr. Low high-density lipoprotein cholesterol as a risk factor in coronary heart disease: a working group report. Circulation 2001; 103: 2213-2218.
DOI: 10.1161/01.cir.103.17.2213
Google Scholar
[4]
Huang ZP, Inazu A, Nohara A, Higashikata T, Mabuchi H. Cholesteryl ester transfer protein inhibitor (JTT-705) and the development of atherosclerosis in rabbits with severe hypercholesterolaemia. Clinical Science 2002; 103: 587-594.
DOI: 10.1042/cs1030587
Google Scholar
[5]
Assmann G, Schulte H, von Eckardstein A, Huang Y. High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. The PROCAM experience and pathophysiological implications for reverse cholesterol transport. Atherosclerosis 1996; 124: 11-20 (Suppl. ).
DOI: 10.1016/0021-9150(96)05852-2
Google Scholar
[6]
Forte TM, McCall MR. The role of apolipoprotein A-I-containing lipoproteins in atherosclerosis. Curr Opin Lipidol 1994; 5: 354-364.
Google Scholar
[7]
Duriez P, Fruchart JC. High-density lipoprotein subclasses and apolipoprotein A-I. Clin Chim Acta 1999; 286(1-2): 97-114.
DOI: 10.1016/s0009-8981(99)00096-0
Google Scholar
[8]
Paszty C, Maeda N, Verstuyft J, Rubin EM. Apolipoprotein AI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice. J Clin Invest 1994; 94: 899-903.
DOI: 10.1172/jci117412
Google Scholar
[9]
Liu AC, Lawn RM, Verstuyft JG, Rubin EM. Human apolipoprotein A-I prevents atherosclerosis associated with apolipoprotein[a] in transgenic mice. J Lipid Res 1994; 35: 2263-2267.
DOI: 10.1016/s0022-2275(20)39932-6
Google Scholar
[10]
Plump AS, Scott CJ, Breslow JL. Human apolipoprotein A-I gene expression increases high-density lipoprotein and suppresses atherosclerosis in the apolipoprotein E-deficient mouse. Proc Natl Acad Sci USA 1994; 91: 9607-9611.
DOI: 10.1073/pnas.91.20.9607
Google Scholar
[11]
Balakumar P, Rose M, Singh M. PPAR ligands: are they potential agents for cardiovascular disorders? Pharmacology 2007; 80(1): 1-10.
DOI: 10.1159/000102594
Google Scholar
[12]
Alkhalaf M. Resveratrol-induced apoptosis is associated with activation of p.53 and inhibition of protein translation in T47D human breast cancer cells. Pharmacology 2007; 80(2-3): 134-43.
DOI: 10.1159/000103253
Google Scholar
[13]
Guo L, Lian JH, Ji W, Hu WR, Wu GL, Gong BQ. Establishment of a cell-based drug screening system for identifying selective down-regulators of mPGES-1. Inflamm Res 2006; 55: 114-118.
DOI: 10.1007/s00011-005-0061-x
Google Scholar
[14]
Guo L, Hu RW, Lian JH, Ji W, Deng T, Qian M, Gong BQ. Anti-hyperlipidemic properties of CM108 (a flavone derivative) in vitro and in vivo. Eur J Pharmacol 2006; 551(1-3): 80-6.
DOI: 10.1016/j.ejphar.2006.08.048
Google Scholar
[15]
Staels B, Vu-Dac N, Kosykh VA, Saladin R, Fruchart JC, Dallongeville J, Auwerx J. Fibrates down-regulate apolipoprotein C-III expression independent of induction of peroxisomal acyl co-enzyme A oxidase. J Clin Invest 1995; 65: 705-712.
DOI: 10.1172/jci117717
Google Scholar
[16]
van Raalte DH, Li M, Pritchard PH, Wasan KM. Peroxisome proliferator-activated receptor (PPAR)-alpha: a pharmacological target with a promising future. Pharm Res 2004; 21(9): 1531-8.
DOI: 10.1023/b:pham.0000041444.06122.8d
Google Scholar