Recent studies call into question the necessity of hypertrophic growth of the heart as a "compensatory" response to hemodynamic stress. These findings, coupled with recent progress in dissecting the molecular bases of hypertrophy, raise the prospect of suppressing hypertrophy without provoking circulatory insufficiency. In this article, we focus on signaling pathways that hold promise as potential targets for therapeutic intervention. We also summarize observations from animal models and clinical trials that suggest benefit from an antihypertrophic strategy.
机构:
Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan
Akazawa, H
Komuro, I
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机构:
Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan
机构:
Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan
Akazawa, H
Komuro, I
论文数: 0引用数: 0
h-index: 0
机构:
Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan