Gemfibrozil decreases atherosclerosis in experimental diabetes in association with a reduction in oxidative stress and inflammation

[1]  M. Cooper,et al.  Rosiglitazone Attenuates Atherosclerosis in a Model of Insulin Insufficiency Independent of Its Metabolic Effects , 2005, Arteriosclerosis, thrombosis, and vascular biology.

[2]  Axel Haverich,et al.  Angiotensin II induces MMP-2 in a p47phox-dependent manner. , 2005, Biochemical and biophysical research communications.

[3]  A. Shah,et al.  Peroxisome Proliferator–Activated Receptor &agr; Induces NADPH Oxidase Activity in Macrophages, Leading to the Generation of LDL with PPAR-&agr; Activation Properties , 2004 .

[4]  D. Gábor,et al.  The Levels of Soluble Adhesion Molecules in Diabetic and Nondiabetic Patients with Combined Hyperlipoproteinemia and the Effect of Ciprofibrate Therapy , 2004, Angiology.

[5]  T. Ide,et al.  Enhancement of insulin signaling through inhibition of tissue lipid accumulation by activation of peroxisome proliferator-activated receptor (PPAR) alpha in obese mice. , 2004, Medical science monitor : international medical journal of experimental and clinical research.

[6]  F. Colpaert,et al.  Cardiovascular drugs inhibit MMP-9 activity from human THP-1 macrophages. , 2004, DNA and cell biology.

[7]  M. Cooper,et al.  Imatinib Attenuates Diabetes-Associated Atherosclerosis , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[8]  J. Rossi,et al.  Regulation of monocyte chemoattractant protein-1 by the oxidized lipid, 13-hydroperoxyoctadecadienoic acid, in vascular smooth muscle cells via nuclear factor–kappa B (NF-кB) , 2004 .

[9]  M. Cooper,et al.  Irbesartan but Not Amlodipine Suppresses Diabetes-Associated Atherosclerosis , 2004, Circulation.

[10]  A. Shah,et al.  Peroxisome proliferator-activated receptor alpha induces NADPH oxidase activity in macrophages, leading to the generation of LDL with PPAR-alpha activation properties. , 2004, Circulation research.

[11]  J. Hamada,et al.  Induction of Tissue Factor Expression in Endothelial Cells by Basic Fibroblast Growth Factor and its Modulation by Fenofibric acid , 2003, Thrombosis journal.

[12]  J. Borensztajn,et al.  The peroxisome-proliferator-activated receptor alpha agonist ciprofibrate severely aggravates hypercholesterolaemia and accelerates the development of atherosclerosis in mice lacking apolipoprotein E. , 2003, The Biochemical journal.

[13]  M. Reitman,et al.  Peroxisome proliferator-activated receptor-alpha agonist treatment in a transgenic model of type 2 diabetes reverses the lipotoxic state and improves glucose homeostasis. , 2003, Diabetes.

[14]  Steven M. Holland,et al.  Mechanical Stretch Enhances mRNA Expression and Proenzyme Release of Matrix Metalloproteinase‐2 (MMP‐2) via NAD(P)H Oxidase‐Derived Reactive Oxygen Species , 2003, Circulation research.

[15]  Y. Chao,et al.  Reduction of Atherosclerosis by the Peroxisome Proliferator-activated Receptor α Agonist Fenofibrate in Mice* , 2002, The Journal of Biological Chemistry.

[16]  E. Schiffrin,et al.  PPARα Activator Effects on Ang II–Induced Vascular Oxidative Stress and Inflammation , 2002 .

[17]  D. Playford,et al.  Effect of fenofibrate on brachial artery flow-mediated dilatation in type 2 diabetes mellitus. , 2002, The American journal of cardiology.

[18]  T. Kislinger,et al.  RAGE Blockade Stabilizes Established Atherosclerosis in Diabetic Apolipoprotein E–Null Mice , 2002, Circulation.

[19]  J. Rutledge,et al.  Angiotensin II is associated with activation of NF-kappaB-mediated genes and downregulation of PPARs. , 2002, Physiological genomics.

[20]  M. Cooper,et al.  Prevention of Accelerated Atherosclerosis by Angiotensin-Converting Enzyme Inhibition in Diabetic Apolipoprotein E–Deficient Mice , 2002, Circulation.

[21]  BjörnFagerberg,et al.  Circulating Oxidized LDL Is Associated With Subclinical Atherosclerosis Development and Inflammatory Cytokines (AIR Study) , 2002 .

[22]  M. Nieminen,et al.  Peroxisome proliferator-activated receptor alpha gene variants influence progression of coronary atherosclerosis and risk of coronary artery disease. , 2002, Circulation.

[23]  E. Schiffrin,et al.  PPARalpha activator effects on Ang II-induced vascular oxidative stress and inflammation. , 2002, Hypertension.

[24]  M. Andrassy,et al.  Diabetes-associated sustained activation of the transcription factor nuclear factor-kappaB. , 2001, Diabetes.

[25]  V. D’Agati,et al.  Receptor for Advanced Glycation End Products Mediates Inflammation and Enhanced Expression of Tissue Factor in Vasculature of Diabetic Apolipoprotein E–Null Mice , 2001, Arteriosclerosis, thrombosis, and vascular biology.

[26]  C. Semenkovich,et al.  PPARalpha deficiency reduces insulin resistance and atherosclerosis in apoE-null mice. , 2001, The Journal of clinical investigation.

[27]  Diabetes Atherosclerosis Intervention Study Investigators Effect of fenofibrate on progression of coronary-artery disease in type 2 diabetes: the Diabetes Atherosclerosis Intervention Study, a randomised study , 2001, The Lancet.

[28]  A. van Tol,et al.  Proatherogenic Role of Elevated CE Transfer From HDL to VLDL1 and Dense LDL in Type 2 Diabetes: Impact of the Degree of Triglyceridemia , 2001, Arteriosclerosis, thrombosis, and vascular biology.

[29]  B. Jude,et al.  PPARα Agonists Inhibit Tissue Factor Expression in Human Monocytes and Macrophages , 2001 .

[30]  D. Haskard,et al.  Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1–Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation , 2001, Circulation.

[31]  T. Awata,et al.  The ligands/activators for peroxisome proliferator-activated receptor α (PPARα) and PPARγ increase Cu2+, Zn2+-superoxide dismutase and decrease p22phox message expressions in primary endothelial cells , 2001 .

[32]  T. Awata,et al.  The ligands/activators for peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma increase Cu2+,Zn2+-superoxide dismutase and decrease p22phox message expressions in primary endothelial cells. , 2001, Metabolism: clinical and experimental.

[33]  B. Jude,et al.  PPARalpha agonists inhibit tissue factor expression in human monocytes and macrophages. , 2001, Circulation.

[34]  R. Evans,et al.  Role for Peroxisome Proliferator-Activated Receptor &agr; in Oxidized Phospholipid–Induced Synthesis of Monocyte Chemotactic Protein-1 and Interleukin-8 by Endothelial Cells , 2000, Circulation research.

[35]  Bruno Derudas,et al.  Peroxisome Proliferator-activated Receptor α Activators Improve Insulin Sensitivity and Reduce Adiposity* , 2000, The Journal of Biological Chemistry.

[36]  A. Tedgui,et al.  CLA-1/SR-BI is expressed in atherosclerotic lesion macrophages and regulated by activators of peroxisome proliferator-activated receptors. , 2000, Circulation.

[37]  K. Channon,et al.  Vascular superoxide production by NAD(P)H oxidase: association with endothelial dysfunction and clinical risk factors. , 2000, Circulation research.

[38]  S. Jackson,et al.  Ciprofibrate therapy improves endothelial function and reduces postprandial lipemia and oxidative stress in type 2 diabetes mellitus. , 2000, Circulation.

[39]  D. Sorescu,et al.  NAD(P)H oxidase: role in cardiovascular biology and disease. , 2000, Circulation research.

[40]  C. Cimminiello,et al.  Effects of gemfibrozil on insulin sensitivity and on haemostatic variables in hypertriglyceridemic patients. , 2000, Atherosclerosis.

[41]  J. Berger,et al.  Activation of PPARα or γ Reduces Secretion of Matrix Metalloproteinase 9 but Not Interleukin 8 from Human Monocytic THP-1 Cells , 2000 .

[42]  G. Zhou,et al.  Activation of PPARalpha or gamma reduces secretion of matrix metalloproteinase 9 but not interleukin 8 from human monocytic THP-1 cells. , 2000, Biochemical and biophysical research communications.

[43]  W. Daniel,et al.  Angiotensin II-induced superoxide anion generation in human vascular endothelial cells: role of membrane-bound NADH-/NADPH-oxidases. , 1999, Cardiovascular research.

[44]  K. Birkeland,et al.  Serum levels of advanced glycation end products are increased in patients with type 2 diabetes and coronary heart disease. , 1999, Diabetes care.

[45]  W. Hsueh,et al.  Peroxisome proliferator-activated receptor activators target human endothelial cells to inhibit leukocyte-endothelial cell interaction. , 1999, Arteriosclerosis, thrombosis, and vascular biology.

[46]  T. Wilt,et al.  Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. , 1999, The New England journal of medicine.

[47]  V. McGovern Exploring the topography of physiological genomics. , 1999, Physiological genomics.

[48]  B. Rollins,et al.  Monocyte chemoattractant protein-1 accelerates atherosclerosis in apolipoprotein E-deficient mice. , 1999, Arteriosclerosis, thrombosis, and vascular biology.

[49]  A. Hamsten,et al.  Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variables to progression of coronary artery disease in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT). , 1998, Journal of the American College of Cardiology.

[50]  J Auwerx,et al.  Mechanism of action of fibrates on lipid and lipoprotein metabolism. , 1998, Circulation.

[51]  B. Staels,et al.  Activation of Proliferator-activated Receptors α and γ Induces Apoptosis of Human Monocyte-derived Macrophages* , 1998, The Journal of Biological Chemistry.

[52]  J. Gamble,et al.  Factors influencing the ability of HDL to inhibit expression of vascular cell adhesion molecule-1 in endothelial cells. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[53]  W. Koenig,et al.  Activation of human aortic smooth-muscle cells is inhibited by PPARα but not by PPARγ activators , 1998, Nature.

[54]  P. Libby,et al.  Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion stabilization. , 1998, Circulation.

[55]  S. Noji,et al.  Expression of peroxisome proliferator-activated receptor alpha (PPAR alpha) in primary cultures of human vascular endothelial cells. , 1998, Biochemical and biophysical research communications.

[56]  R. Holman,et al.  Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: United Kingdom prospective diabetes study (UKPDS: 23) , 1998, BMJ.

[57]  W. Koenig,et al.  Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators. , 1998, Nature.

[58]  M. Nieminen,et al.  Prevention of the angiographic progression of coronary and vein-graft atherosclerosis by gemfibrozil after coronary bypass surgery in men with low levels of HDL cholesterol. Lopid Coronary Angiography Trial (LOCAT) Study Group. , 1997, Circulation.

[59]  A. Schmidt,et al.  Characterization and Functional Analysis of the Promoter of RAGE, the Receptor for Advanced Glycation End Products* , 1997, The Journal of Biological Chemistry.

[60]  G. Paolisso,et al.  Oxidative Stress and Diabetic Vascular Complications , 1996, Diabetes Care.

[61]  P. Libby,et al.  Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. , 1994, The Journal of clinical investigation.

[62]  W. Cefalu,et al.  Glycohemoglobin measured by automated affinity HPLC correlates with both short-term and long-term antecedent glycemia. , 1994, Clinical chemistry.

[63]  M. Wolin,et al.  Inhibition of coronary artery superoxide dismutase attenuates endothelium-dependent and -independent nitrovasodilator relaxation. , 1991, Circulation research.

[64]  G. Macdonald,et al.  Reduction of Blood Pressure by Puromycin Infused Selectively into the Ischaemic Kidney in Experimental Renal Hypertension , 1967 .

[65]  R. Klein,et al.  Effects of Temperature, Na and K Concentration and Quinidine on Transmembrane Flux of K42 and Incidence of Atrial Fibrillation , 1958, Circulation research.

[66]  A. Gutman,et al.  Incorporation of glycine nitrogen into uric acid in normal and gouty man. , 1952, Metabolism: clinical and experimental.