The vascular biology of atherosclerosis.

[1]  M. Daemen,et al.  Atherosclerotic plaque rupture: local or systemic process? , 2003, Arteriosclerosis, thrombosis, and vascular biology.

[2]  J. Beckman,et al.  Peroxisome proliferator activated receptor gamma and its activation in the treatment of insulin resistance and atherosclerosis: issues and opportunities , 2003, Current opinion in cardiology.

[3]  J. Plutzky.  PPARs as Therapeutic Targets: Reverse Cardiology? , 2003, Science.

[4]  G. Reaven.  The insulin resistance syndrome , 2003, Current atherosclerosis reports.

[5]  W. Koenig,et al.  Antidiabetic PPAR&ggr;-Activator Rosiglitazone Reduces MMP-9 Serum Levels in Type 2 Diabetic Patients With Coronary Artery Disease , 2003 .

[6]  S. Haffner,et al.  Effect of Rosiglitazone Treatment on Nontraditional Markers of Cardiovascular Disease in Patients With Type 2 Diabetes Mellitus , 2002, Circulation.

[7]  P. Libby,et al.  Inflammation and Atherosclerosis , 2002, Circulation.

[8]  T. Akasaka,et al.  Impact of troglitazone on coronary stent implantation using small stents in patients with type 2 diabetes mellitus. , 2002, The American journal of cardiology.

[9]  S. Perrey,et al.  Peroxisome proliferator-activated receptors , 2002, Current atherosclerosis reports.

[10]  E. Creemers,et al.  This Review Is Part of a Thematic Series on Matrix Metalloproteinases, Which Includes the following Articles: Matrix Metalloproteinase Inhibition after Myocardial Infarction: a New Approach to Prevent Heart Failure? Matrix Metalloproteinase: Regulation and Dysregulation in the failing Heart Matrix M , 2022 .

[11]  A. Tedgui,et al.  Anti-Inflammatory Mechanisms in the Vascular Wall , 2001, Circulation research.

[12]  W. Hsueh,et al.  Troglitazone Inhibits Formation of Early Atherosclerotic Lesions in Diabetic and Nondiabetic Low Density Lipoprotein Receptor–Deficient Mice , 2001, Arteriosclerosis, thrombosis, and vascular biology.

[13]  S. Perrey,et al.  Troglitazone Inhibits Atherosclerosis in Apolipoprotein E–Knockout Mice: Pleiotropic Effects on CD36 Expression and HDL , 2001, Arteriosclerosis, thrombosis, and vascular biology.

[14]  Christopher K. Glass,et al.  Atherosclerosis The Road Ahead , 2001, Cell.

[15]  J. Auwerx,et al.  Reduction of atherosclerosis in apolipoprotein E knockout mice by activation of the retinoid X receptor , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[16]  G. Tomkin,et al.  Abnormalities in apo B‐containing lipoproteins in diabetes and atherosclerosis , 2001, Diabetes/metabolism research and reviews.

[17]  J. Schrezenmeir,et al.  Postprandial triglycerides and endothelial function. , 2001, Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association.

[18]  M. Jaye,et al.  PPAR-α and PPAR-γ activators induce cholesterol removal from human macrophage foam cells through stimulation of the ABCA1 pathway , 2001, Nature Medicine.

[19]  D. Altshuler,et al.  The role of PPAR-γ in macrophage differentiation and cholesterol uptake , 2001, Nature Medicine.

[20]  R. Evans,et al.  PPAR-γ dependent and independent effects on macrophage-gene expression in lipid metabolism and inflammation , 2001, Nature Medicine.

[21]  T. Akasaka,et al.  Troglitazone reduces neointimal tissue proliferation after coronary stent implantation in patients with non-insulin dependent diabetes mellitus: a serial intravascular ultrasound study. , 2000, Journal of the American College of Cardiology.

[22]  H. Ginsberg,et al.  The Insulin Resistance Syndrome: Impact on Lipoprotein Metabolism and Atherothrombosis , 2000, Journal of cardiovascular risk.

[23]  Andrew C. Li,et al.  Oxidized LDL reduces monocyte CCR2 expression through pathways involving peroxisome proliferator-activated receptor gamma. , 2000, The Journal of clinical investigation.

[24]  A. Schmidt,et al.  Atherosclerosis and diabetes: The rage connection , 2000, Current atherosclerosis reports.

[25]  C. Rogers,et al.  The comparative pathobiology of atherosclerosis and restenosis. , 2000, The American journal of cardiology.

[26]  Andrew C. Li,et al.  Peroxisome proliferator–activated receptor γ ligands inhibit development of atherosclerosis in LDL receptor–deficient mice , 2000 .

[27]  E. Fleck,et al.  Peroxisome proliferator-activated receptor and retinoid X receptor ligands inhibit monocyte chemotactic protein-1-directed migration of monocytes. , 2000, European journal of pharmacology.

[28]  P. Libby,et al.  Peroxisome Proliferator-Activated Receptor-γ Activators Inhibit IFN-γ-Induced Expression of the T Cell-Active CXC Chemokines IP-10, Mig, and I-TAC in Human Endothelial Cells1 , 2000, The Journal of Immunology.

[29]  W. Hsueh,et al.  Expression and Function of PPARγ in Rat and Human Vascular Smooth Muscle Cells , 2000 .

[30]  P. Libby.  Changing concepts of atherogenesis , 2000, Journal of internal medicine.

[31]  D. Bishop-Bailey.  Peroxisome proliferator‐activated receptors in the cardiovascular system , 2000, British journal of pharmacology.

[32]  Shokei Kim,et al.  Molecular and cellular mechanisms of angiotensin II-mediated cardiovascular and renal diseases. , 2000, Pharmacological reviews.

[33]  T. Willson,et al.  The PPARs: from orphan receptors to drug discovery. , 2000, Journal of medicinal chemistry.

[34]  U. Förstermann,et al.  Nitric oxide in the pathogenesis of vascular disease , 2000, The Journal of pathology.

[35]  V. Pasceri,et al.  Modulation of vascular inflammation in vitro and in vivo by peroxisome proliferator-activated receptor-gamma activators. , 2000, Circulation.

[36]  G. Natoli,et al.  Anti-inflammatory cyclopentenone prostaglandins are direct inhibitors of IκB kinase , 2000, Nature.

[37]  P. Groot,et al.  Chemokines and atherosclerosis. , 1999, Atherosclerosis.

[38]  C. Glass,et al.  The peroxisome proliferator‐activated receptorγ (PPARγ) as a regulator of monocyte/macrophage function , 1999 .

[39]  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.

[40]  J. Plutzky,et al.  Atherosclerotic plaque rupture: emerging insights and opportunities. , 1999, The American journal of cardiology.

[41]  T. Hla,et al.  Endothelial Cell Apoptosis Induced by the Peroxisome Proliferator-activated Receptor (PPAR) Ligand 15-Deoxy-Δ12,14-prostaglandin J2 * , 1999, The Journal of Biological Chemistry.

[42]  J F Cornhill,et al.  Prevalence and extent of atherosclerosis in adolescents and young adults: implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth Study. , 1999, JAMA.

[43]  R. Ross,et al.  Atherosclerosis is an inflammatory disease. , 1998, American heart journal.

[44]  P. Libby,et al.  Peroxisome proliferator-activated receptor gamma activators inhibit gene expression and migration in human vascular smooth muscle cells. , 1998, Circulation research.

[45]  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.

[46]  P. Libby,et al.  Macrophages in Human Atheroma Contain PPARγ: Differentiation-Dependent Peroxisomal Proliferator-Activated Receptor γ (PPARγ) Expression and Reduction of MMP-9 Activity through PPARγ Activation in Mononuclear Phagocytes in Vitro , 1998 .

[47]  S. Tanaka,et al.  Potent inhibitory effect of troglitazone on carotid arterial wall thickness in type 2 diabetes. , 1998, The Journal of clinical endocrinology and metabolism.

[48]  R. Evans,et al.  PPARγ Promotes Monocyte/Macrophage Differentiation and Uptake of Oxidized LDL , 1998, Cell.

[49]  R. Evans,et al.  Oxidized LDL Regulates Macrophage Gene Expression through Ligand Activation of PPARγ , 1998, Cell.

[50]  B. Spiegelman.  PPARγ in Monocytes: Less Pain, Any Gain? , 1998, Cell.

[51]  U. Laufs,et al.  Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors. , 1998, Circulation.

[52]  A. Luster,et al.  Chemokines--chemotactic cytokines that mediate inflammation. , 1998, The New England journal of medicine.

[53]  G. Struhl,et al.  Regulation of the Hedgehog and Wingless signalling pathways by the F-box/WD40-repeat protein Slimb , 1998, Nature.

[54]  B. Seed,et al.  PPAR-γ agonists inhibit production of monocyte inflammatory cytokines , 1998, Nature.

[55]  Christopher K. Glass,et al.  The peroxisome proliferator-activated receptor-γ is a negative regulator of macrophage activation , 1998, Nature.

[56]  M. Laakso,et al.  Epidemiology of risk factors for cardiovascular disease in diabetes and impaired glucose tolerance. , 1997, Atherosclerosis.

[57]  T. Lüscher,et al.  Biology of the Endothelium , 1997, Clinical cardiology.

[58]  T. Collins,et al.  Hemodynamics, Endothelial Gene Expression, and Atherogenesis a , 1997, Annals of the New York Academy of Sciences.

[59]  J P Cooke,et al.  Nitric oxide synthase: role in the genesis of vascular disease. , 1997, Annual review of medicine.

[60]  D. Faxon,et al.  Troglitazone inhibits vascular smooth muscle cell growth and intimal hyperplasia. , 1996, The Journal of clinical investigation.

[61]  T. Springer.  Traffic signals for lymphocyte recirculation and leukocyte emigration: The multistep paradigm , 1994, Cell.

[62]  Monteiro Jg.  Atherosclerosis and diabetes , 1957 .