E3 ubiquitin ligase RNF5 attenuates pathological cardiac hypertrophy through STING.
E3 ubiquitin ligase RNF5 attenuates pathological cardiac hypertrophy through STING.
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E3泛素连接酶RNF5通过STING减轻病理性心脏肥大
DOI：
10.1038/s41419-022-05231-8
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发表时间：
2022-10-21
影响因子：
9
通讯作者：
Zhang, Yan-Zhou
中科院分区：
文献类型：
--
作者：
Yang, Lu-Lu;Xiao, Wen-Chang;Li, Huan;Hao, Zheng-Yang;Liu, Gui-Zhi;Zhang, Dian-Hong;Wu, Lei-Ming;Wang, Zheng;Zhang, Yan-Qing;Huang, Zhen;Zhang, Yan-Zhou
环指蛋白5（Ring-finger protein 5，RNF5）是一种E3泛素连接酶，在多种人体组织中表达。RNF5参与调节内质网应激、炎症和天然免疫，在多种肿瘤的发生发展中发挥重要作用。然而，RNF5在心肌肥厚中的作用尚未报道。在本研究中，我们发现RNF5在病理性心肌肥厚小鼠心脏中的表达增加。功能丧失研究表明，RNF5缺乏会加剧心脏肥大，而功能获得研究表明，RNF5的过度表达具有相反的作用。干扰素基因刺激因子（stimulator of interferon genes，STING）是一种能够激活I型干扰素免疫的信号分子，在多种疾病中参与炎症和免疫反应。蛋白质-蛋白质相互作用实验证实STING与RNF5相互作用。进一步的研究表明，RNF5通过K48连接的多聚泛素化促进STING降解来抑制心肌肥大。因此，我们将RNF5定义为心脏肥大的重要调节信号。
Ring-finger protein 5 (RNF5) is an E3 ubiquitin ligase which is expressed in a variety of human tissues. RNF5 is involved in the regulation of endoplasmic reticulum stress, inflammation, and innate immunity and plays an important role in the occurrence and development of various tumors. However, the role of RNF5 in cardiac hypertrophy has not been reported. In this study, we found the expression of RNF5 was increased in the hearts of mice with pathological cardiac hypertrophy. The loss-of-function research demonstrated that RNF5 deficiency exacerbated cardiac hypertrophy, whereas gain-of-function studies revealed that overexpression of RNF5 had opposite effects. The stimulator of interferon genes (STING) is a signaling molecule that can activate type I interferon immunity, which can meditate inflammation and immune response in many diseases. The protein–protein interaction experiments confirmed that STING interacted with RNF5. Further studies showed that RNF5 inhibited cardiac hypertrophy by promoting STING degradation through K48-linked polyubiquitination. Therefore, we defined RNF5 as importantly regulated signaling for cardiac hypertrophy.
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