Relationship between Advanced Glycation End Products and Plaque Progression in Patients with Acute Coronary Syndrome: The JAPAN-ACS Sub-study

[1]  D. Nathan,et al.  The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Study at 30 Years: Overview , 2013, Diabetes Care.

[2]  M. Matsuzaki,et al.  High HbA1c levels correlate with reduced plaque regression during statin treatment in patients with stable coronary artery disease: Results of the coronary atherosclerosis study measuring effects of rosuvastatin using intravascular ultrasound in Japanese subjects (COSMOS) , 2012, Cardiovascular Diabetology.

[3]  E. Mathiesen,et al.  The metabolic syndrome and progression of carotid atherosclerosis over 13 years. The Tromsø study , 2012, Cardiovascular Diabetology.

[4]  Ruiyan Zhang,et al.  Insulin resistance predicts progression of de novo atherosclerotic plaques in patients with coronary heart disease: a one-year follow-up study , 2012, Cardiovascular Diabetology.

[5]  T. Imaizumi,et al.  Serum levels of advanced glycation end products (AGEs) are independent correlates of insulin resistance in nondiabetic subjects. , 2012, Cardiovascular therapeutics.

[6]  Peter Libby,et al.  Effect of two intensive statin regimens on progression of coronary disease. , 2011, The New England journal of medicine.

[7]  Sho-ichi Yamagishi,et al.  Role of advanced glycation end products (AGEs) and receptor for AGEs (RAGE) in vascular damage in diabetes , 2011, Experimental Gerontology.

[8]  S. Yamagishi,et al.  Pigment epithelium-derived factor (PEDF) inhibits proximal tubular cell injury in early diabetic nephropathy by suppressing advanced glycation end products (AGEs)-receptor (RAGE) axis. , 2011, Pharmacological research.

[9]  M. Matsuzaki,et al.  More intensive lipid lowering is associated with regression of coronary atherosclerosis in diabetic patients with acute coronary syndrome--sub-analysis of JAPAN-ACS study. , 2010, Journal of atherosclerosis and thrombosis.

[10]  Kohjiro Ueki,et al.  Report of the Committee on the Classification and Diagnostic Criteria of Diabetes Mellitus , 2010, Journal of diabetes investigation.

[11]  Hongmei Yu,et al.  Alteration of T helper cell subsets in the optic nerve of experimental autoimmune encephalomyelitis. , 2010, International journal of molecular medicine.

[12]  M. Matsuzaki,et al.  Diabetes mellitus is a major negative determinant of coronary plaque regression during statin therapy in patients with acute coronary syndrome--serial intravascular ultrasound observations from the Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome Trial (the JAPAN-ACS Tria , 2010, Circulation journal : official journal of the Japanese Circulation Society.

[13]  Zhidan Luo,et al.  Resveratrol prevents the impairment of advanced glycosylation end products (AGE) on macrophage lipid homeostasis by suppressing the receptor for AGE via peroxisome proliferator-activated receptor gamma activation. , 2010, International journal of molecular medicine.

[14]  A. Einstein,et al.  A Novel Monoclonal Antibody for RAGE-Directed Imaging Identifies Accelerated Atherosclerosis in Diabetes , 2010, Journal of Nuclear Medicine.

[15]  Tsukasa Suzuki,et al.  Positive association of serum levels of advanced glycation end products and high mobility group box-1 with asymmetric dimethylarginine in nondiabetic chronic kidney disease patients. , 2009, Metabolism: clinical and experimental.

[16]  Qi Zhang,et al.  Decreased serum esRAGE level is associated with angiographically determined coronary plaque progression in diabetic patients. , 2009, Clinical biochemistry.

[17]  Katsumi Miyauchi,et al.  Effect of intensive statin therapy on regression of coronary atherosclerosis in patients with acute coronary syndrome: a multicenter randomized trial evaluated by volumetric intravascular ultrasound using pitavastatin versus atorvastatin (JAPAN-ACS [Japan assessment of pitavastatin and atorvastatin , 2009, Journal of the American College of Cardiology.

[18]  Merlin C. Thomas,et al.  Receptor for Advanced Glycation End Products (RAGE) Deficiency Attenuates the Development of Atherosclerosis in Diabetes , 2008, Diabetes.

[19]  S. Yamagishi,et al.  Possible involvement of tobacco-derived advanced glycation end products (AGEs) in an increased risk for developing cancers and cardiovascular disease in former smokers. , 2008, Medical hypotheses.

[20]  E. Tuzcu,et al.  Effect of diabetes on progression of coronary atherosclerosis and arterial remodeling: a pooled analysis of 5 intravascular ultrasound trials. , 2008, Journal of the American College of Cardiology.

[21]  M. Cooper,et al.  The role of AGEs in cardiovascular disease. , 2008, Current pharmaceutical design.

[22]  K. Chayama,et al.  Elevated levels of serum advanced glycation end products in patients with non‐alcoholic steatohepatitis , 2007, Journal of gastroenterology and hepatology.

[23]  Raimund Erbel,et al.  Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. , 2006, JAMA.

[24]  Y. Zou,et al.  Receptor for Advanced-Glycation End Products: Key Modulator of Myocardial Ischemic Injury , 2006, Circulation.

[25]  A. Schmermund,et al.  Relationship Between Cardiovascular Risk as Predicted by Established Risk Scores Versus Plaque Progression as Measured by Serial Intravascular Ultrasound in Left Main Coronary Arteries , 2004, Circulation.

[26]  K. Shimada,et al.  Early Statin Treatment in Patients With Acute Coronary Syndrome: Demonstration of the Beneficial Effect on Atherosclerotic Lesions by Serial Volumetric Intravascular Ultrasound Analysis During Half a Year After Coronary Event: The ESTABLISH Study , 2004, Circulation.

[27]  Ann Marie Schmidt,et al.  Protein Glycation: A Firm Link to Endothelial Cell Dysfunction , 2004, Circulation research.

[28]  Paul Schoenhagen,et al.  Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. , 2004, JAMA.

[29]  D. O'leary,et al.  Intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. , 2003, The New England journal of medicine.

[30]  Merlin C. Thomas,et al.  A Breaker of Advanced Glycation End Products Attenuates Diabetes‐Induced Myocardial Structural Changes , 2003, Circulation research.

[31]  H. Vlassara,et al.  Diabetes and advanced glycation endproducts , 2002, Journal of internal medicine.

[32]  M. Brownlee.  Biochemistry and molecular cell biology of diabetic complications , 2001, Nature.

[33]  C. Tracy,et al.  American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. , 2001, Journal of the American College of Cardiology.

[34]  R. Bucala,et al.  Immunological Evidence that Non-carboxymethyllysine Advanced Glycation End-products Are Produced from Short Chain Sugars and Dicarbonyl Compounds in vivo , 2000, Molecular medicine.

[35]  O H Førde,et al.  The Tromsø Study. Distribution and population determinants of gamma-glutamyltransferase. , 1990, American journal of epidemiology.

[36]  R. Levy,et al.  Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. , 1972, Clinical chemistry.

[37]  P. Marraccini,et al.  Inverse association between circulating levels of soluble receptor for advanced glycation end-products and coronary plaque burden. , 2012, Journal of atherosclerosis and thrombosis.