The effects of dipeptidyl peptidase-4 on cardiac fibrosis in pressure overload-induced heart failure.

[1]  Y. Sakurai,et al.  Renoprotective effects of a dipeptidyl peptidase 4 inhibitor in a mouse model of progressive renal fibrosis , 2017, Renal failure.

[2]  S. Rajagopalan,et al.  Dipeptidyl peptidase-4 inhibition: insights from the bench and recent clinical studies , 2016, Current opinion in lipidology.

[3]  I. Komuro,et al.  DPP-4 inhibition has beneficial effects on the heart after myocardial infarction. , 2016, Journal of molecular and cellular cardiology.

[4]  D. Drucker,et al.  Inhibition of Dipeptidyl Peptidase-4 Impairs Ventricular Function and Promotes Cardiac Fibrosis in High Fat–Fed Diabetic Mice , 2015, Diabetes.

[5]  Ryan A Frieler,et al.  Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling. , 2015, Circulation.

[6]  Na-Hyung Kim,et al.  The Nonglycemic Actions of Dipeptidyl Peptidase-4 Inhibitors , 2014, BioMed research international.

[7]  C. Vinel,et al.  CD4+ T Cells Promote the Transition From Hypertrophy to Heart Failure During Chronic Pressure Overload , 2014, Circulation.

[8]  Y. Ishigaki,et al.  Linagliptin-Mediated DPP-4 Inhibition Ameliorates Kidney Fibrosis in Streptozotocin-Induced Diabetic Mice by Inhibiting Endothelial-to-Mesenchymal Transition in a Therapeutic Regimen , 2014, Diabetes.

[9]  A. Avogaro,et al.  Dipeptidyl-peptidase 4 Inhibition: Linking Metabolic Control to Cardiovascular Protection , 2014, Current pharmaceutical design.

[10]  M. Mocanu,et al.  Dipeptidyl peptidase-4 inhibitors and GLP-1 reduce myocardial infarct size in a glucose-dependent manner , 2013, Cardiovascular Diabetology.

[11]  Deepak L. Bhatt,et al.  Saxagliptin and cardiovascular outcomes in patients with type 2 diabetes mellitus. , 2013, The New England journal of medicine.

[12]  M. Su,et al.  DPP4 Deficiency Exerts Protective Effect against H2O2 Induced Oxidative Stress in Isolated Cardiomyocytes , 2013, PloS one.

[13]  高橋 彩子.  Dipeptidyl-peptidase IV inhibition improves pathophysiology of heart failure and increases survival rate in pressure-overloaded mice , 2013 .

[14]  P. Abete,et al.  Treatment for chronic heart failure in the elderly: current practice and problems , 2013, Heart Failure Reviews.

[15]  T. Murohara,et al.  Dipeptidyl Peptidase-4 Modulates Left Ventricular Dysfunction in Chronic Heart Failure via Angiogenesis-Dependent and -Independent Actions , 2012, Circulation.

[16]  D. Drucker,et al.  Natriuretic effect by exendin-4, but not the DPP-4 inhibitor alogliptin, is mediated via the GLP-1 receptor and preserved in obese type 2 diabetic mice. , 2012, American journal of physiology. Renal physiology.

[17]  Limei Liu,et al.  Dipeptidyl Peptidase 4 Inhibitor Sitagliptin Protects Endothelial Function in Hypertension Through a Glucagon–Like Peptide 1–Dependent Mechanism , 2012, Hypertension.

[18]  J. Korinek,et al.  Variable phenotype in murine transverse aortic constriction. , 2012, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

[19]  Liang Liu,et al.  Dipeptidyl Peptidase-4 Inhibitor Sitagliptin Protects Endothelial Function in Hypertension through GLP-1 Dependent Mechanism , 2012 .

[20]  I. Komuro,et al.  Effects of pitavastatin on pressure overload-induced heart failure in mice. , 2012, Circulation journal : official journal of the Japanese Circulation Society.

[21]  R. D. de Boer,et al.  Early and late effects of the DPP-4 inhibitor vildagliptin in a rat model of post-myocardial infarction heart failure , 2011, Cardiovascular diabetology.

[22]  A. Owens,et al.  The year in heart failure. , 2011, Journal of the American College of Cardiology.

[23]  L. Rossoni,et al.  Dipeptidyl peptidase IV inhibition attenuates blood pressure rising in young spontaneously hypertensive rats , 2011, Journal of hypertension.

[24]  C. Morimoto,et al.  Inhibition of dipeptidyl peptidase 4 regulates microvascular endothelial growth induced by inflammatory cytokines. , 2010, Biochemical and biophysical research communications.

[25]  E. Jackson.  Dipeptidyl peptidase IV inhibition alters the hemodynamic response to angiotensin-converting enzyme inhibition in humans with the metabolic syndrome. , 2010, Hypertension.

[26]  F. Reis,et al.  Effects of Sitagliptin Treatment on Dysmetabolism, Inflammation, and Oxidative Stress in an Animal Model of Type 2 Diabetes (ZDF Rat) , 2010, Mediators of inflammation.

[27]  M. Mehra,et al.  Chronic heart failure: contemporary diagnosis and management. , 2010, Mayo Clinic proceedings.

[28]  Lawrence A Leiter,et al.  The incretin system and cardiometabolic disease. , 2010, The Canadian journal of cardiology.

[29]  Vijay G Divakaran,et al.  Adaptive and Maladptive Effects of SMAD3 Signaling in the Adult Heart After Hemodynamic Pressure Overloading , 2009, Circulation. Heart failure.

[30]  O. Tarnavski.  Mouse surgical models in cardiovascular research. , 2009, Methods in molecular biology.

[31]  N. Frangogiannis,et al.  Characterization of the inflammatory and fibrotic response in a mouse model of cardiac pressure overload , 2009, Histochemistry and Cell Biology.

[32]  M. Hori,et al.  Inhibition of Cardiac Remodeling by Pravastatin Is Associated with Amelioration of Endoplasmic Reticulum Stress , 2008, Hypertension Research.

[33]  E. Heath,et al.  Hypoxia-inducible factor-1 target genes as indicators of tumor vessel response to vascular endothelial growth factor inhibition. , 2008, Cancer research.

[34]  R. Bolli,et al.  Stromal Cell–Derived Factor-1&agr; Confers Protection Against Myocardial Ischemia/Reperfusion Injury: Role of the Cardiac Stromal Cell–Derived Factor-1&agr;–CXCR4 Axis , 2007 .

[35]  R. Bolli,et al.  Stromal cell derived factor-1 alpha confers protection against myocardial ischemia/reperfusion injury: role of the cardiac stromal cell derived factor-1 alpha CXCR4 axis. , 2007, Circulation.

[36]  M. Siddiqui,et al.  Inhibition of Jak2 phosphorylation attenuates pressure overload cardiac hypertrophy. , 2006, Vascular pharmacology.

[37]  P. Whittaker,et al.  Collagen and picrosirius red staining: a polarized light assessment of fibrillar hue and spatial distribution , 2005 .

[38]  E. Olson,et al.  Cardiac hypertrophy: the good, the bad, and the ugly. , 2003, Annual review of physiology.

[39]  I. Komuro,et al.  3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors prevent the development of cardiac hypertrophy and heart failure in rats. , 2003, Journal of molecular and cellular cardiology.

[40]  H P Schultheiss,et al.  Dilated cardiomyopathy is associated with significant changes in collagen type I/III ratio. , 1999, Circulation.

[41]  R. Jaenisch,et al.  Type III collagen is crucial for collagen I fibrillogenesis and for normal cardiovascular development. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[42]  A. Katz.  The Cardiomyopathy of Overload: An Unnatural Growth Response in the Hypertrophied Heart , 1994, Annals of Internal Medicine.

[43]  J. Ross,et al.  Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[44]  E. Frohlich.  Cardiac hypertrophy in hypertension. , 1987, The New England journal of medicine.