{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T05:48:07Z","timestamp":1776923287322,"version":"3.51.2"},"reference-count":20,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2022,7,6]],"date-time":"2022-07-06T00:00:00Z","timestamp":1657065600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["No. 81300230"],"award-info":[{"award-number":["No. 81300230"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Laboratory Analysis"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The development of cardiac fibrosis involves the activation of cardiac fibroblasts (CFs) and their differentiation into myofibroblasts, which leads to the disruption of the extracellular matrix network. In the past few years, microRNAs (miRNA) have been described as potential targets for treating cardiac diseases. Although miR\u2010338\u20103p has been shown to participate in the development of carcinoma, whether it affects cardiac fibrosis is unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We examined the expression profiles of microRNAs in left ventricular samples of heart failure mice established by thoracic aortic constriction (TAC). Real\u2010time quantitative reverse transcription polymerase chain reaction (qRT\u2010PCR) was used to detect the expression of miR\u2010338\u20103p. CCK\u20108 assay\/Transwell migration assay was used to measure the proliferation rate\/migration of CFs. Luciferase reporter gene assay was used to test the binding between miR\u2010338\u20103p and FGFR2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>This study demonstrated that miR\u2010338\u20103p was significantly decreased in thoracic aortic constriction mice. Cardiac miR\u2010338\u20103p amounts were also reduced in patients with dilated cardiomyopathy (DCM). Interestingly, miR\u2010338\u20103p overexpression inhibited \u03b1\u2010SMA, COL1A1, and COL3A1 expression, as well as cell proliferation and migration in CFs. Bioinformatics analysis and dual\u2010luciferase reporter assays revealed FGFR2 was targeted by miR\u2010338\u20103p, whose antifibrotic effect could be alleviated by overexpression of FGFR2. Moreover, in DCM cases, serum miR\u2010338\u20103p levels were markedly elevated in individuals with worse outcomes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The present study provides evidence that miR\u2010338\u20103p suppresses cardiac fibroblast activation, proliferation, and migration by directly targeting FGFR2 in mice. Besides, serum miR\u2010338\u20103p might constitute a potential prognostic biomarker of dilated cardiomyopathy.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcla.24584","type":"journal-article","created":{"date-parts":[[2022,7,6]],"date-time":"2022-07-06T11:31:55Z","timestamp":1657107115000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["<scp>MicroRNA<\/scp>\u2010338\u20103p as a therapeutic target in cardiac fibrosis through <scp>FGFR2<\/scp> suppression"],"prefix":"10.1002","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2561-4431","authenticated-orcid":false,"given":"Cheng","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Cardiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences Guangdong Cardiovascular Institute  Guangzhou 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