| http://purl.uniprot.org/citations/28871329 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28871329 | http://www.w3.org/2000/01/rdf-schema#comment | "Atrial fibrillation (AF) is associated with atrial fibrosis. Inhibition of atrial fibrosis might be a plausible approach for AF prevention and therapy. This study is designed to evaluate the potential role of CD44, a membrane receptor known to regulate fibrosis, and its related signaling in the pathogenesis of atrial fibrosis and AF. Treatment of cultured rat atrial fibroblasts with transforming growth factor-β (TGF-β, a key mediator of atrial fibrosis) led to a higher expression of hyaluronan (HA), CD44, STAT3, and collagen (a principal marker of fibrosis) than that of ventricular fibroblasts. In vivo, TGF-β transgenic mice and AF patients exhibited a greater expression of HA, CD44, STAT3, and collagen in their atria than wild-type mice and sinus rhythm subjects, respectively. Treating TGF-β transgenic mice with an anti-CD44 blocking antibody resulted in a lower expression of STAT3 and collagen in their atria than those with control IgG antibody. Programmed stimulation triggered less AF episodes in TGF-β transgenic mice treated with anti-CD44 blocking antibody than in those with control IgG. Blocking CD44 signaling with anti-CD44 antibody and mutated CD44 plasmids attenuated TGF-β-induced STAT3 activation and collagen expression in cultured atrial fibroblasts. Deletion and mutational analysis of the collagen promoter along with chromatin immunoprecipitation demonstrated that STAT3 served as a vital transcription factor in collagen expression. TGF-β-mediated HA/CD44/STAT3 pathway plays a crucial role in the development of atrial fibrosis and AF. Blocking CD44-dependent signaling may be a feasible way for AF management."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.org/dc/terms/identifier | "doi:10.1007/s00395-017-0647-9"xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/author | "Chang S.H."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/author | "Chen W.J."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/author | "Kuo C.T."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/author | "Lee J.L."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/author | "Hsu Y.J."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/author | "Yeh Y.H."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/name | "Basic Res Cardiol"xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/pages | "58"xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/title | "Transforming growth factor-beta-mediated CD44/STAT3 signaling contributes to the development of atrial fibrosis and fibrillation."xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://purl.uniprot.org/core/volume | "112"xsd:string |
| http://purl.uniprot.org/citations/28871329 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28871329 |
| http://purl.uniprot.org/citations/28871329 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/28871329 |
| http://purl.uniprot.org/uniprot/#_A0A078BBI5-mappedCitation-28871329 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28871329 |
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| http://purl.uniprot.org/uniprot/#_A0A0K2JZP0-mappedCitation-28871329 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28871329 |
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