Defective Ca<sup>2+</sup> Cycling as a Key Pathogenic Mechanism of Heart Failure

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  • Yano Masafumi
    Department of Medicine and Clinical Science, Division of Cardiology, Yamaguchi University Graduate School of Medicine
  • Yamamoto Takeshi
    Department of Medicine and Clinical Science, Division of Cardiology, Yamaguchi University Graduate School of Medicine
  • Kobayashi Shigeki
    Department of Medicine and Clinical Science, Division of Cardiology, Yamaguchi University Graduate School of Medicine
  • Ikeda Yasuhiro
    Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine
  • Matsuzaki Masunori
    Department of Medicine and Clinical Science, Division of Cardiology, Yamaguchi University Graduate School of Medicine

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  • Defective Ca2+ cycling as a key pathogenic mechanism of heart failure

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Abstract

Structural and functional alterations in the Ca2+ regulatory proteins present in the sarcoplasmic reticulum (SR) have recently been shown to play a crucial role in the pathogenesis of heart failure (HF), and lethal arrhythmia as well. Chronic activation of the sympathetic nervous system induces abnormalities in both the function and structure of these proteins. For instance, the diastolic Ca2+ leak through the SR Ca2+ release channel (ryanodine receptor) reduces the SR Ca2+ content, inducing contractile dysfunction. Moreover, the Ca2+ leak provides a substrate for delayed afterdepolarization that leads to lethal arrhythmia. There is a considerable body of evidence regarding the role of Ca2+ cycling abnormality in HF. (Circ J 2008; Suppl A: A-22 - A-30)<br>

Journal

  • Circulation Journal

    Circulation Journal 72 (SupplementA), A22-A30, 2008

    The Japanese Circulation Society

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