Effects of Pitavastatin on Pressure Overload-Induced Heart Failure in Mice

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著者

    • KAMEDA Yoshihito
    • Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine
    • HASEGAWA Hiroshi
    • Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine
    • KUBOTA Akihiko
    • Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine
    • TADOKORO Hiroyuki
    • Department of Bio-Medical Engineering, Tokai University School of High-Technology for Human Welfare
    • KOBAYASHI Yoshio
    • Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine
    • KOMURO Issei
    • Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine
    • TAKANO Hiroyuki
    • Department of Molecular Cardiovascular Pharmacology, Graduate School of Pharmaceutical Sciences, Chiba University

抄録

<b><i>Background:</i></b> 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart. <b><i>Methods and Results:</i></b> C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC. <b><i>Conclusions:</i></b> Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart. (<i>Circ J</i> 2012; <b>76:</b> 1159-1168)<br>

収録刊行物

  • Circulation journal : official journal of the Japanese Circulation Society

    Circulation journal : official journal of the Japanese Circulation Society 76(5), 1159-1168, 2012-04-25

    The Japanese Circulation Society

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各種コード

  • NII論文ID(NAID)
    10030132534
  • NII書誌ID(NCID)
    AA11591968
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13469843
  • データ提供元
    CJP書誌  CJP引用  J-STAGE 
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