{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T23:01:24Z","timestamp":1767826884240,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2023,11,9]],"date-time":"2023-11-09T00:00:00Z","timestamp":1699488000000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2023,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>The aim of this study was to elucidate the mechanism of beraprost sodium (BPS) in the intervention of myocardial fibrosis after myocardial infarction (MI) through glycogen synthase kinase\u20103\u03b2 (GSK\u20103\u03b2) and to provide new ideas for intervention in myocardial fibrosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>MI model rats given BPS and cardiac fibroblasts (CFs) treated with BPS and TGF\u2010\u03b2. HE staining and Masson staining were used to detect the pathological changes of myocardial tissue. Fibrotic markers were detected by immunohistochemical staining. The expressions of GSK\u20103\u03b2, cAMP response element binding protein (CREB), and p\u2010CREB were analyzed by qPCR and western blot analysis. EDU\u00a0staining was used to detect the proliferation of CFs. The promoter activity of GSK\u20103\u03b2 was detected by luciferase assay. Chromatin immunoprecipitation assay was used to detect the binding levels of GSK\u20103\u03b2 promoter and Y\u2010box binding protein 1 (YBX1). The levels of intracellular cyclic adenosine monophosphate (cAMP) were analyzed by enzyme\u2010linked immunosorbent assay (ELISA).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>After operation, BPS improved myocardial fibrosis and upregulated GSK\u20103\u03b2 protein expression in male SD rats. BPS can down\u2010regulate \u03b1\u2010smooth muscle actin (\u03b1\u2010SMA) level and up\u2010regulate GSK\u20103\u03b2 protein expression in CFs after TGF\u2010\u03b2 stimulation. Furthermore, GSK\u20103\u03b2 knockdown can reverse the effect of BPS on TGF\u2010\u03b2\u2010activated CFs, enhance \u03b1\u2010SMA expression, and promote the proliferation of CFs. BPS could regulate GSK\u20103\u03b2 expression by promoting the binding of GSK\u20103\u03b2 promoter to YBX1. BPS induced upregulation of p\u2010CREB and cAMP, resulting in reduced fibrosis, which was reversed by the knockdown of GSK\u20103\u03b2 or prostaglandin receptor (IPR) antagonists.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>BPS treatment increased the binding of YBX1 to the GSK\u20103\u03b2 promoter, and GSK\u20103\u03b2 protein expression was upregulated, which further caused the upregulation of p\u2010CREB and cAMP, and finally inhibited myocardial fibrosis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/iid3.1050","type":"journal-article","created":{"date-parts":[[2023,11,9]],"date-time":"2023-11-09T11:07:16Z","timestamp":1699528036000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Beraprost sodium attenuates the development of myocardial fibrosis after myocardial infarction by regulating GSK\u20103\u03b2 expression in 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