{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T14:51:36Z","timestamp":1781189496834,"version":"3.54.1"},"reference-count":33,"publisher":"S. Karger AG","issue":"4","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiology"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Objective:&lt;\/i&gt;&lt;\/b&gt; To explore the role of platelet-derived growth factor-B (PDGF-B)\/platelet-derived growth factor receptor-\u03b2 (PDGFR-\u03b2) signaling in chronic atrial fibrillation (AF). &lt;b&gt;&lt;i&gt;Methods:&lt;\/i&gt;&lt;\/b&gt; Thirty-nine AF patients and 33 patients with sinus rhythm (SR) were enrolled. Twenty canines were randomized into 5 groups: control, sham and AF lasting 1, 2 or 4 weeks. The AF canine models were made by rapid atrial pacing. Rat atrial fibroblasts were treated with PDGF-BB or PDGF-BB + PDGFR inhibitor AG1295, respectively. Gene expression in the right atrial appendage of patients, the left atrium of canines and rat atrial fibroblasts was measured by quantitative real-time PCR and Western blot, respectively. The degree of atrial fibrosis was evaluated by Masson trichrome staining. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; The degree of atrial fibrosis and the expression of PDGF-B, PDGFR-\u03b2 and collagen type I (COL1) in AF patients significantly increased compared to patients with SR. The degree of atrial fibrosis and the expression of PDGF-B and COL1 in canines increased progressively with the increased duration of AF. The expression of PDGFR-\u03b2 increased progressively 2 weeks after AF. PDGF-BB promoted the proliferation and COL1 secretion of rat atrial fibroblasts. AG1295 attenuated these effects. &lt;b&gt;&lt;i&gt;Conclusions:&lt;\/i&gt;&lt;\/b&gt; Our study suggests that PDGF-B\/PDGFR-\u03b2 signaling, which promotes the proliferation and COL1 secretion of atrial fibroblasts, is an important contributor to atrial fibrosis in AF and may represent a novel target for the intervention of AF.<\/jats:p>","DOI":"10.1159\/000442940","type":"journal-article","created":{"date-parts":[[2016,1,11]],"date-time":"2016-01-11T22:01:18Z","timestamp":1452549678000},"page":"242-256","source":"Crossref","is-referenced-by-count":16,"title":["The Role of Platelet-Derived Growth Factor-B\/Platelet-Derived Growth Factor Receptor-\u03b2 Signaling in Chronic Atrial 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