Anti-Atherosclerotic Molecules Targeting Oxidative Stress and Inflammation

被引:38
作者
Adameova, A.
Xu, Y. J.
Duhamel, T. A.
Tappia, P. S.
Shan, L.
Dhalla, N. S. [1 ]
机构
[1] St Boniface Gen Hosp, Res Ctr, Inst Cardiovasc Sci, Winnipeg, MB R2H 2A6, Canada
关键词
Atherosclerosis; inflammation; oxidative stress; statins; fibrates; novel anti-atherosclerotic drugs; ESTER TRANSFER PROTEIN; HIGH-DENSITY-LIPOPROTEIN; HMG-COA REDUCTASE; CHOLESTEROL ACYLTRANSFERASE INHIBITOR; ANGIOTENSIN-CONVERTING ENZYME; ACTIVATED-RECEPTOR-GAMMA; CORONARY-HEART-DISEASE; REDOX-SENSITIVE GENES; SMOOTH-MUSCLE-CELLS; ACYL-COA;
D O I
10.2174/138161209789058048
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The accumulation of lipids within arteries remains to be the initial impulse for the pathogenesis of atherosclerosis; however, both inflammation and oxidative stress are considered to play a critical role in this process. Several lipid lowering drugs are used as the first line therapy in atherosclerosis; however, different agents have been found to exhibit beneficial effects which are independent of their lipid lowering activity. Both statins and fibrates have been reported to exert anti-inflammatory and anti-oxidative effects in addition to their anti-atherosclerotic actions. Furthermore, anti-hypertensive, anti-diabetic and anti-platelet drugs, which reduce oxidative stress and inflammation, have been shown to attenuate atherosclerosis. In addition, novel substances such as HDL-related agents, cyclopentenone prostaglandins, lipoprotein-associated phospholipase A(2) inhibitors, 5-lipoxygenase pathway inhibitors, acyl CoA: cholesterol acyltransferase inhibitors, analogues of probucol and lysophosphatidic acid antagonists have been developed for the treatment of atherosclerosis as a consequence of their actions on oxidative stress and inflammation. The present article reviews the involvement of inflammation and oxidative stress in the pathogenesis of atherosclerosis and focuses on the mechanisms of some clinically used as well as potential anti-atherosclerotic substances with anti-inflammatory and anti-oxidative properties.
引用
收藏
页码:3094 / 3107
页数:14
相关论文
共 159 条
[11]   Rationale for prescription omega-3-acid ethyl ester therapy for hypertriglyceridemia: A primer for clinicians [J].
Bays, Harold .
DRUGS OF TODAY, 2008, 44 (03) :205-246
[12]  
Berk Bradford C, 2007, Trans Am Clin Climatol Assoc, V118, P209
[13]   HMG-CoA reductase and ACAT inhibitors act synergistically to lower plasma cholesterol and limit atherosclerotic lesion development in the cholesterol-fed rabbit [J].
Bocan, TMA ;
Mueller, SB ;
Brown, EQ ;
Lee, P ;
Bocan, MJ ;
Rea, T ;
Pape, ME .
ATHEROSCLEROSIS, 1998, 139 (01) :21-30
[14]   The ACAT inhibitor avasimibe reduces macrophages and matrix metalloproteinase expression in atherosclerotic lesions of hypercholesterolemic rabbits [J].
Bocan, TMA ;
Krause, BR ;
Rosebury, WS ;
Mueller, SB ;
Lu, XK ;
Dagle, C ;
Major, T ;
Lathia, C ;
Lee, H .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (01) :70-79
[15]   Torcetrapib and carotid intima-media thickness in mixed dyslipidaemia (RADIANCE 2 study): a randomised, double-blind trial [J].
Bots, Michiel L. ;
Visseren, Frank L. ;
Evans, Gregory W. ;
Riley, Ward A. ;
Revkin, James H. ;
Tegeler, Charles H. ;
Shear, Charles L. ;
Duggan, William T. ;
Vicari, Ralph M. ;
Grobbee, Diederick E. ;
Kastelein, John J. .
LANCET, 2007, 370 (9582) :153-160
[16]   Effects of cholesteryl ester transfer protein inhibition on high-density lipoprotein subspecies, apolipoprotein A-I metabolism, and fecal sterol excretion [J].
Brousseau, ME ;
Diffenderfer, MR ;
Millar, JS ;
Nartsupha, C ;
Asztalos, BF ;
Welty, FK ;
Wolfe, ML ;
Rudling, M ;
Björkhem, I ;
Angelin, B ;
Mancuso, JP ;
Digenio, AG ;
Rader, DJ ;
Schaefer, EJ .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2005, 25 (05) :1057-1064
[17]   Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol [J].
Brousseau, ME ;
Schaefer, EJ ;
Wolfe, ML ;
Bloedon, LT ;
Digenio, AG ;
Clark, RW ;
Mancuso, JP ;
Rader, DJ .
NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (15) :1505-1515
[18]  
Cabrero A., 2002, Current Drug Targets - Inflammation and Allergy, V1, P243, DOI 10.2174/1568010023344616
[19]  
Chang CCY, 2000, J BIOL CHEM, V275, P28083
[20]   Lysophosphatidic acid-induced interleukin-1β expression is mediated through Gi/Rho and the generation of reactive oxygen species in macrophages [J].
Chang, Chi-Lun ;
Lin, Mu-En ;
Hsu, Hsien-Yeh ;
Yao, Chao-Ling ;
Hwang, Shiaw-Min ;
Pan, Chien-Yuan ;
Hsu, Chi-Yen ;
Lee, Hsinyu .
JOURNAL OF BIOMEDICAL SCIENCE, 2008, 15 (03) :357-363