IRF3 regulates cardiac fibrosis but not hypertrophy in mice during angiotensin II-induced hypertension.

在血管紧张素 II 诱导的高血压期间，IRF3 调节小鼠的心脏纤维化，但不调节心肌肥厚。

• 批准号: 21790710
• 负责人: TSUSHIMA Kensuke
• 金额: $ 2.83万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21790710/
• 关键词: 心臓; 線維化; 炎症; アンギオテンシンII; IRF3; Fibrocyte; 心肥大

Hypertension is a typical modern lifestyle-related disease that is closely associated with the development of cardiovascular disorders. Elevation of angiotensin II (ANG II) is one of several critical factors for hypertension and heart failure ; however, the mechanisms underlying the ANG II-mediated pathogenesis are still poorly understood. Here, we show that ANG II-mediated cardiac fibrosis, but not hypertrophy, is regulated by interferon regulatory factor3(IRF3), which until now has been exclusively studied in the innate immune system. Our present study reveals an unrecognized function of IRF3 in cardiac remodeling, providing new insight into the progression of hypertension-induced cardiac pathogenesis.

高血压是一种典型的现代生活方式相关疾病，与心血管疾病的发展密切相关。血管紧张素II（ANG II）的升高是高血压和心力衰竭的几个关键因素之一;然而，ANG II介导的发病机制仍然知之甚少。在这里，我们表明，血管紧张素II介导的心脏纤维化，但不是肥大，是由干扰素调节因子3（IRF 3），这到目前为止，已专门研究了先天免疫系统。我们目前的研究揭示了IRF 3在心脏重构中未被认识的功能，为高血压诱导的心脏发病机制的进展提供了新的见解。

项目成果

IRF3 regulates cardiac fibrosis but not hypertrophy in mice during angiotensin II-induced hypertension

• DOI: 10.1096/fj.10-174615
• 发表时间: 2011-05-01
• 期刊: FASEB JOURNAL
• 影响因子: 4.8
• 作者: Tsushima, Kensuke;Osawa, Tomoko;Nagai, Ryozo
• 通讯作者: Nagai, Ryozo