Hui Wang, Wenhua Su, Shuojie Zhang, Lulin Wang, Panpan Zhao, Tongtong Zhang, Xiaoli Xie, Juhua Dan
Laboratory of Molecular Genetics of Aging & Tumor, Medical School, Kunming University of Science and Technology, Kunming, Yunnan, China.
Department of Cardiology, The First People's Hospital of Yunnan Province, Kunming, Yunnan, China.
Int J Cardiol Heart Vasc. 2023 Sep 20;48:101271. doi: 10.1016/j.ijcha.2023.101271. eCollection 2023 Oct.
Cardiac hypertrophy is initially an adaptive response to physiological and pathological stimuli. Although pathological myocardial hypertrophy is the main cause of morbidity and mortality, our understanding of its mechanism is still weak. NFAT3 (nuclear factor of activated T-cell-3) is a member of the nuclear factor of the activated T cells (NFAT) family. NFAT3 plays a critical role in regulating the expression of cardiac hypertrophy genes by inducing their transcription. Recently, accumulating evidence has indicated that NFAT3 is a potent regulator of the progression of cardiac hypertrophy. This review, for the first time, summarizes the current studies on NFAT3 in cardiac hypertrophy, including the pathophysiological processes and the underlying pathological mechanism, focusing on the nuclear translocation and transcriptional function of NFAT3. This review will provide deep insight into the pathogenesis of cardiac hypertrophy and a theoretical basis for identifying new therapeutic targets in the NFAT3 network.
心脏肥大最初是对生理和病理刺激的一种适应性反应。尽管病理性心肌肥大是发病和死亡的主要原因,但我们对其机制的了解仍然有限。NFAT3(活化T细胞核因子3)是活化T细胞核因子(NFAT)家族的成员。NFAT3通过诱导心脏肥大基因的转录,在调节其表达方面发挥关键作用。最近,越来越多的证据表明,NFAT3是心脏肥大进展的有力调节因子。本综述首次总结了目前关于NFAT3在心脏肥大方面的研究,包括病理生理过程和潜在的病理机制,重点关注NFAT3的核转位和转录功能。本综述将为深入了解心脏肥大的发病机制以及为在NFAT3网络中确定新的治疗靶点提供理论依据。