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Atrial fibrosis is an important pathophysiological contributor to AF. This study aimed to investigate the role of the clustered miR\u201023b\u20103p and miR\u201027b\u20103p in atrial fibrosis. Human atrial fibroblasts (HAFs) were isolated from atrial appendage tissue of patients with sinus rhythm. A cell model of atrial fibrosis was achieved in Ang\u2010II\u2010induced HAFs. Cell proliferation and migration were detected. We found that miR\u201023b\u20103p and miR\u201027b\u20103p were markedly increased in atrial appendage tissues of AF patients and in Ang\u2010II\u2010treated HAFs. Overexpression of miR\u201023b\u20103p and miR\u201027b\u20103p enhanced the expression of collagen, type I, alpha 1 (COL1A1), COL3A1 and ACTA2 in HAFs without significant effects on their proliferation and migration. Luciferase assay showed that miR\u201023b\u20103p and miR\u201027b\u20103p targeted two different sites in 3\u02b9\u2010UTR of transforming growth factor (TGF)\u2010\u03b21 receptor 3 (TGFBR3) respectively. Consistently, TGFBR3 siRNA could increase fibrosis\u2010related genes expression, along with the Smad1 inactivation and Smad3 activation in HAFs. Additionally, overexpression of TGFBR3 could alleviate the increase of COL1A1, COL3A1 and ACTA2 in HAFs after transfection with miR\u201023b\u20103p and miR\u201027b\u20103p respectively. Moreover, Smad3 was activated in HAFs in response to Ang\u2010II treatment and inactivation of Smad3 attenuated up\u2010regulation of miR\u201023b\u20103p and miR\u201027b\u20103p in Ang\u2010II\u2010treated HAFs. Taken together, these results suggest that the clustered miR\u201023b\u20103p and miR\u201027b\u20103p consistently promote atrial fibrosis by targeting TGFBR3 to activate Smad3 signalling in HAFs, suggesting that miR\u201023b\u20103p and miR\u201027b\u20103p are potential therapeutic targets for atrial fibrosis.<\/jats:p>","DOI":"10.1111\/jcmm.14211","type":"journal-article","created":{"date-parts":[[2019,2,7]],"date-time":"2019-02-07T09:31:03Z","timestamp":1549531863000},"page":"3246-3256","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Novel role of the clustered miR\u201023b\u20103p and miR\u201027b\u20103p in enhanced expression of fibrosis\u2010associated genes by targeting TGFBR3 in atrial fibroblasts"],"prefix":"10.1111","volume":"23","author":[{"given":"Zhenzhen","family":"Yang","sequence":"first","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Clinical Pharmacology Guangdong Cardiovascular 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