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

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)升高是高血压和心力衰竭的几个关键因素之一；然而，Ang II介导的发病机制仍不清楚。在这里，我们表明血管紧张素II介导的心肌纤维化，而不是肥大，是由干扰素调节因子3(IRF3)调节的，到目前为止，它只在先天性免疫系统中进行研究。我们目前的研究揭示了IRF3在心脏重塑中一个未知的功能，为高血压引起的心脏发病机制的进展提供了新的视角。

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.