3 research outputs found

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

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    Dipeptidyl peptidase-4 (DPP-4) inhibitors are hypoglycemic agents. DPP-4 inhibitor has cardioprotective effects after transverse aortic constriction (TAC), but role of DPP-4 on cardiac fibrosis after TAC is not well known. Our aim was to determine the effects of DPP-4 on cardiac fibrosis in murine TAC model. Wild-type mice and DPP-4 knockout mice were subjected to TAC. Wild-type mice were then treated with vehicle or DPP-4 inhibitor. DPP-4 activities in serum and heart tissue were significantly increased at 2 weeks after TAC, but they were significantly decreased by DPP-4 inhibitor treatment. The inhibition of DPP-4 did not affect left ventricular hypertrophy, but improved cardiac function and decreased myocardial and perivascular fibrosis after TAC. The inhibition of DPP-4 decreased the collagen type III/I ratio in myocardium. These results suggest that DPP-4 inhibition ameliorates the progression of heart failure after TAC by changing the quality and quantity of cardiac fibrosis

    カクチョウガタ シンキンショウ ニ タイスル カリュウジョウ コロニー シゲキ インシ オ モチイタ ヒシンシュウセイ サイセイ イリョウ ノ チョウセン

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    平成15年度-平成17年度年度科学研究費補助金 (基盤研究(A) 一般 循環器内科学 課題番号15209027) 研究成果報告書Li Y. et al., Postinfarction Treatment With an Adenoviral Vector Expressing Hepatocyte Growth Factor Relieves Chronic Left Ventricular Remodeling and Dysfunction in Mice. Circulation. 2003 107(19): 2499-2506Hayakawa K. et al., Inhibition of Granulation Tissue Cell Apoptosis During the Subacute Stage of Myocardial Infarction Improves Cardiac Remodeling and Dysfunction at the Chronic Stage. Circulation. 2003 108(1): 104-109Wang N. et al., Antidiabetic Drug Miglitol Inhibits Myocardial Apoptosis Involving Decreased Hydroxyl Radical Production and Bax Expression in an Ischaemia/Reperfusion Rabbit Heart. British Journal of Pharmacology. 2004 142(6): 983-990Minatoguchi S. et al., Acceleration of the Healing Process and Myocardial Regeneration May Be Important as a Mechanism of Improvement of Cardiac Function and Remodeling by Postinfarction Granulocyte Colony-Stimulating Factor Treatment. Circulation. 2004 109(21): 2572-2580Kawai T. et al., Efficient Cardiomyogenic Differentiation of Embryonic Stem Cell by Fibroblast Growth Factor 2 and Bone Morphogenetic Protein 2. Circulation Journal. 2004 68(7): 691-702Li Y. et al., Critical Roles for the Fas/Fas Ligand System in Postinfarction Ventricular Remodeling and Heart Failure. Circulation Research. 2004 95(6): 627-636Ikoma T. et al., A Definitive Role of RhoC in Metastasis of Orthotopic Lung Cancer in Mice. Clinical Cancer Research. 2004 10(3): 1192-1200Takemura G. et al., Role of Apoptosis in Remodeling after Myocardial Infarction. Pharmacology & Therapeutics. 2004 104(1): 1-16Okada H. et al., Postinfarction Gene Therapy Against Transforming Growth Factor-β Signal Modulates Infarct Tissue Dynamics and Attenuates Left Ventricular Remodeling and Heart Failure. Circulation. 2005 111(19): 2430-2437Misao Y. et al., Cyclophosphamide Improves the Function of Post-Infarct Hearts by Reducing Old Infarct Area and Accelerating the Mobilization of CD34+ Cells. Circulation Journal. 2005 69(6): 763-765Nagano S. et al., An Efficient Construction of Conditionally Replicating Adenoviruses that Target Tumor Cells with Multiple Factors. Gene Therapy. 2005 12(18): 1385-1393Ushikori H. et al., Local Overexpression of HB-EGF Exacerbates Remodeling Following Myocardial Infarction by Activating Noncardiomyocytes. Laboratory Investigation. 2005 85(7): 862-873Miyata S. et al., Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor. American Journal of Pathology. 2006 168(2): 386-397Li Y. et al., Treatment with Granulocyte Colony-Stimulating Factor Ameliorates Chronic Heart Failure. Laboratory Investigation. 2006 86(1): 32-4
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