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Volumn 9, Issue 9, 2008, Pages 950-956

HDL: Still a target for new therapies?

Author keywords

Atherosclerosis; Cardiovascular disease; HDL; Risk factor

Indexed keywords

APOLIPOPROTEIN A1; ATORVASTATIN; CHOLESTEROL ESTER TRANSFER PROTEIN; CHOLESTEROL ESTER TRANSFER PROTEIN INHIBITOR; CSL 111; ETC 216; FIBRIC ACID DERIVATIVE; HIGH DENSITY LIPOPROTEIN; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; LAROPIPRANT; LOW DENSITY LIPOPROTEIN CHOLESTEROL; NICOTINIC ACID; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA AGONIST; PIOGLITAZONE; ROSUVASTATIN; TORCETRAPIB; UNCLASSIFIED DRUG;

EID: 50249169416     PISSN: 14724472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Review
Times cited : (17)

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    • Bots ML, Visseren FL, Evans GW, Riley WA, Revkin JH, Tegeler CH, Shear CL, Duggan WT, Vicari RM, Grobbee DE, Kastelein JJ: Torcetrapib and carotid intima-media thickness in mixed dyslipidaemia (RADIANCE 2 study): A randomised, double-blind trial. Lancet (2007) 370(9582):153-160. • This study demonstrated that torcetrapib did not slow the progression of carotid intima-media thickness in patients with mixed dyslipidemia.
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    • This study demonstrated that torcetrapib did not slow the progression of carotid intima-media thickness in patients with familial hypercholesterolemia, •
    • Kastelein JJ, van Leuven SI, Burgess L, Evans GW, Kuivenhoven JA, Barter PJ, Revkin JH, Grobbee DE, Riley WA, Shear CL, Duggan WT et al: Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N Engl J Med (2007) 356(16):1620-1630. • This study demonstrated that torcetrapib did not slow the progression of carotid intima-media thickness in patients with familial hypercholesterolemia.
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    • Kastelein, J.J.1    van Leuven, S.I.2    Burgess, L.3    Evans, G.W.4    Kuivenhoven, J.A.5    Barter, P.J.6    Revkin, J.H.7    Grobbee, D.E.8    Riley, W.A.9    Shear, C.L.10    Duggan, W.T.11
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    • This study demonstrated the effects of torcetrapib on aldosterone levels in animal models, ••
    • Forrest MJ, Bloomfield D, Briscoe RJ, Brown PN, Cumiskey AM, Ehrhart J, Hershey JC, Keller WJ, Ma X, McPherson HE, Messina E et al: Torcetrapib-induced blood pressure elevation is independent of CETP inhibition and is accompanied by increased circulating levels of aldosterone. Br J Pharmacol (2008) 154(7):1465-1473. •• This study demonstrated the effects of torcetrapib on aldosterone levels in animal models.
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    • Davidson M, Meyer PM, Haffner S, Feinstein S, D'Agostino R Sr, Kondos GT, Perez A, Chen Z, Mazzone T: Increased high-density lipoprotein cholesterol predicts the pioglitazone-mediated reduction of carotid intima-media thickness progression in patients with type 2 diabetes mellitus. Circulation (2008) 117(16):2123-2130. •• Raising HDL-C predicts the benefit of pioglitazone, a PPARγ agonist, in slowing the progression of carotid intima-media thickness.
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    • Davidson, M.1    Meyer, P.M.2    Haffner, S.3    Feinstein, S.4    D'Agostino Sr, R.5    Kondos, G.T.6    Perez, A.7    Chen, Z.8    Mazzone, T.9
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    • Zheng L, Nukuna B, Brennan ML, Sun M, Goormastic M, Settle M, Schmitt D, Fu X, Thomson L, Fox PL, Ischiropoulos H et al: Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease. J Clin Invest (2004) 114(4):529-541. • This study demonstrated the role of myeloperoxidase-catalyzed oxidation of apoA-I in the generation of dysfunctional HDL. Inhibition of this pathway may improve the functional quality of HDL, without raising systemic HDL-C levels.
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    • This study demonstrated the role of carbamylation as a chemical pathway involved in the generation of dysfunctional HDL, •
    • Wang Z, Nicholls SJ, Rodriguez ER, Kummu O, Hörkkö S, Barnard J, Reynolds WF, Topol EJ, DiDonato JA, Hazen SL: Protein carbamylation links inflammation, smoking, uremia and atherogenesis. Nat Med (2007) 13(10):1176-1184. • This study demonstrated the role of carbamylation as a chemical pathway involved in the generation of dysfunctional HDL.
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    • Wang, Z.1    Nicholls, S.J.2    Rodriguez, E.R.3    Kummu, O.4    Hörkkö, S.5    Barnard, J.6    Reynolds, W.F.7    Topol, E.J.8    DiDonato, J.A.9    Hazen, S.L.10
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    • Bhattacharyya T, Nicholls SJ, Topol EJ, Zhang R, Yang X, Schmitt D, Fu X, Shao M, Brennan DM, Ellis SG, Brennan ML et al: Relationship of paraoxonase 1 (PON1) gene polymorphisms and functional activity with systemic oxidative stress and cardiovascular risk. J Am Med Assoc (2008) 299(11):1265-1276. •• This study defined the relationship between paraoxonase activity, measures of oxidative stress and cardiovascular risk, and suggested that promoting paraoxonase activity might improve the functional quality of HDL.
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    • An elegant description of the need to focus on the functional quality of HDL, ••
    • deGoma EM, deGoma RL, Rader DJ: Beyond high-density lipoprotein cholesterol levels evaluating high-density lipoprotein function as influenced by novel therapeutic approaches. J Am Coll Cardiol (2008) 51(23):2199-2211. •• An elegant description of the need to focus on the functional quality of HDL.
    • (2008) J Am Coll Cardiol , vol.51 , Issue.23 , pp. 2199-2211
    • deGoma, E.M.1    deGoma, R.L.2    Rader, D.J.3


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