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Tissue thrombin is associated with the pathogenesis of dilated cardiomyopathy

Keiichi Ito1, Kenichi Hongo1, Taro Date1

  • 1Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8, Nishi-shinbashi, Minato-ku, Tokyo 105-8461, Japan.

International Journal of Cardiology
|November 27, 2016
PubMed

Insights

Tissue thrombin contributes to dilated cardiomyopathy (DCM) development. Inhibiting thrombin with dabigatran improved cardiac function and survival in a DCM mouse model, suggesting a potential therapeutic strategy.

Area of Science:

  • Cardiology
  • Biochemistry
  • Pathophysiology

Background:

  • Thrombin, a coagulation cascade product, has roles beyond hemostasis, including gastric contractions and wound healing.
  • Increased coagulability is observed in patients with dilated cardiomyopathy (DCM).
  • This study investigates thrombin's role in DCM pathogenesis.

Purpose of the Study:

  • To clarify the role of thrombin in the pathogenesis of dilated cardiomyopathy (DCM).
  • To explore the potential of thrombin inhibition as a treatment for DCM.

Main Methods:

  • Investigated thrombin expression in human DCM patient hearts and a DCM mouse model (∆K210 knock-in mice).
  • Assessed the effects of dabigatran, a direct thrombin inhibitor, on ∆K210 knock-in mice.
  • Utilized echocardiography, Kaplan-Meier survival analysis, and Western blotting.

Main Results:

  • Strong thrombin expression was detected in heart tissues of DCM patients and ∆K210 knock-in mice.
  • Dabigatran treatment significantly improved fractional shortening in the mice.
  • Dabigatran administration enhanced survival outcomes in the DCM mouse model.

Conclusions:

  • Tissue thrombin plays a role in the pathogenesis of dilated cardiomyopathy (DCM).
  • Thrombin inhibition demonstrates therapeutic potential for treating DCM.
Abstract

Keywords:
Dilated cardiomyopathyDirect thrombin inhibitorThrombin

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