The mechanism of contractile dysfunction in heart failure, focussing on SERCA2a function.

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  • KUSAKARI Yoichiro
    Department of Physiology (II), The Jikei University School of Medicine
  • HIRANO Shuta
    Department of Physiology (II), The Jikei University School of Medicine
  • HONGO Kenichi
    Department of Cardiology, The Jikei University School of Medicine
  • NAKAYAMA Hiroyuki
    Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine
  • OTSU Kinya
    Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine
  • KURIHARA Satoshi
    Department of Physiology (II), The Jikei University School of Medicine

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Other Title
  • 不全心における収縮障害の細胞内メカニズム－ＳＥＲＣＡ２ａを中心として－
  • フゼンシン ニ オケル シュウシュク ショウガイ ノ サイボウ ナイ メカニズム SERCA2a オ チュウシン ト シテ
  • −SERCA2aを中心として−

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Cytosolic Ca2+ is a key regulator of excitation-contraction coupling in myocardium. Myocardial contractile dysfunction in heart failure is characterized by a decrease in contraction and prolonged relaxation. These alterations are mainly due to changes in 1) intracellular Ca2+ transients (CaT), 2) Ca2+ sensitivity of the contractile elements, and/or 3) contractile proteins. It is useful to investigate the relationship between CaT and contraction for understanding of the mechanism of contractile dysfunction in heart failure. There are many reports regarding the alterations in CaT, Ca2+ sensitivity, and contractile proteins in heart failure. Changes in the activity of the sarcoplasmic Ca2+ pump protein, SERCA2a, may be involved in the altered contractility in heart failure. We generated cardiac-restricted overexpression of SERCA2a transgenic mice (TG) and non-transgenic littermates (NTG). To investigate the role of SERCA2a activity for ischemic heart, we used acidosis as a model of acute contractile dysfunction. During acidosis and recovery from acidosis, the peaks of CaT and tension in TG were significantly larger than those in NTG. These results suggest that an increase in the activity of SERCA2a could be beneficial to preserve contractility during acidosis and recovery. Thus, a disturbance of the intracellular Ca2+ homeostasis is one of the key factors for the contractile dysfunction in heart failure.<br>

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