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Updated: Apr 11, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
Periostin as a novel factor responsible for ventricular dilation
Naruto Katsuragi1, Ryuichi Morishita, Noriko Nakamura
1Daiichi Suntory Biomedical Research Ltd, 1-1-1 Wakayamadai Shimamoto-cho, Mishima-gun, Osaka, Japan.
Periostin gene overexpression caused heart failure in rats, leading to cardiac dilation and dysfunction. Inhibiting periostin improved survival and heart function, suggesting it as a potential heart failure treatment target.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Heart Failure Pathophysiology
Background:
- Periostin is upregulated in heart failure myocardium.
- The precise function of periostin in heart failure remains undocumented.
Purpose of the Study:
- To elucidate the role of periostin in heart failure pathogenesis.
- To investigate the effects of periostin gene manipulation in a rat cardiac model.
Main Methods:
- Direct gene transfection (overexpression and antisense inhibition) of periostin in rat hearts.
- Echocardiography and hemodynamic measurements to assess cardiac function.
- Histological analysis for myocyte and collagen changes.
Main Results:
- Periostin overexpression induced left ventricular dilation, impaired cardiac function, myocyte loss, and increased collagen deposition.
- Periostin inhibited myocyte spreading and fibroblast adhesion.
- Inhibition of periostin expression significantly improved survival and cardiac function in a heart failure model.
Conclusions:
- Periostin gene contributes to cardiac dilation and dysfunction in animal models.
- Targeting periostin presents a potential therapeutic strategy for heart failure treatment.
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