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）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。

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.