• Ping Pang, Wei Si, Han Wu, Chunlei Wang, Kuiwu Liu, Yingqiong Jia, Zhengwei Zhang, Feng Zhang, Xue Kong, Yang Yang, Weitao Jiang, Jinglun Song, Linghua Zeng, Yuting Xiong, Jie Lian, Ning Wang, Yu Bian, and Baofeng Yang.
• Department of Pharmacology, College of Basic Medical Sciences, Jilin University, 126 ximin street, Chaoyang District, Changchun, Jilin 130021, China.
• Transl Res. 2023 Jul 1; 257: 304230-42.

AbstractCardiac fibrosis is a common pathological change in the development of heart disease. Circular RNA (circRNA) has been shown to be related to the occurrence and development of various cardiovascular diseases. This study aimed to evaluate the effects and potential mechanisms of circHelz in cardiac fibrosis. Knockdown of circHelz alleviated cardiac fibrosis and myocardial fibroblast activation induced by myocardial infarction (MI) or angiotensin II (AngII) in vivo and transforming growth factor-β (TGF-β) in vitro. Overexpression of circHelz exacerbated cell proliferation and differentiation. Mechanistically, nuclear factor of activated T cells, cytoplasmic 2 (NFATc2) was found to act as a transcriptional activator to upregulate the expression of circHelz. The increased circHelz was demonstrated to bind to Yes-associated protein (YAP) and facilitate its localization in the nucleus to promote cell proliferation and growth. Moreover, silencing YAP1 reversed the detrimental effects caused by circHelz in vitro, as indicated by the observed decreases in cell viability, fibrotic marker expression levels, proliferation and migration. Collectively, the protective effect of circHelz knockdown against cardiac fibrosis injury is accomplished by inhibiting the nuclear translocation of YAP1. Thus, circHelz may be a novel target for the prevention and treatment of cardiovascular disease.Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.

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