Circ_0002295 facilitated myocardial fibrosis progression through the miR-1287/CXCR2 axis

IF 2.9 4区 医学 Q2 Medicine Clinical and Experimental Pharmacology and Physiology Pub Date : 2023-09-09 DOI:10.1111/1440-1681.13819
Guo-Bin Ma, Wen-Xu Chen, Fang-Jie Zhan, Wen-Jing Xie, Rong-Wei Chen, Hong Chen, Wei-Lin Ye, Yu Jiang, Jian-Ping Xu
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Abstract

Myocardial fibrosis (MF) is involved in hypertension, myocardial infarction and heart failure. It has been reported that circular RNA (circRNA) is a key regulatory factor of MF progression. In this study, we revealed that circ_0002295 and CXCR2 were elevated, and miR-1287 was reduced in MF patients. Knockdown of circ_0002295 effectively suppressed the proliferation, migration and MF progression. Circ_0002295 was the molecular sponge of miR-12878, and miR-1287 inhibitor reversed the biological functions of circ_0002295 on the myocardial fibrosis. CXCR2 was a target gene of miR-1287, and CXCR2 silencing relieved the impacts of miR-1287 inhibitor on cardiac myofibroblasts. Circ_0002295 promoted MF progression by regulating the miR-1287/CXCR2 axis, providing a possible circRNA-targeted therapy for MF.

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Circ_0002295通过miR-1287/CXCR2轴促进心肌纤维化进展
心肌纤维化(MF)与高血压、心肌梗死和心力衰竭有关。据报道,环状RNA (circRNA)是MF进展的关键调控因子。在这项研究中,我们发现circ_0002295和CXCR2在MF患者中升高,miR-1287降低。敲低circ_0002295可有效抑制细胞增殖、迁移和MF进展。Circ_0002295是miR-12878的分子海绵,miR-1287抑制剂逆转了Circ_0002295在心肌纤维化中的生物学功能。CXCR2是miR-1287的靶基因,沉默CXCR2可以缓解miR-1287抑制剂对心肌成纤维细胞的影响。Circ_0002295通过调节miR-1287/CXCR2轴促进MF进展,为MF提供了一种可能的circrna靶向治疗方法。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
128
审稿时长
6 months
期刊介绍: Clinical and Experimental Pharmacology and Physiology is an international journal founded in 1974 by Mike Rand, Austin Doyle, John Coghlan and Paul Korner. Our focus is new frontiers in physiology and pharmacology, emphasizing the translation of basic research to clinical practice. We publish original articles, invited reviews and our exciting, cutting-edge Frontiers-in-Research series’.
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