{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:27:16Z","timestamp":1791923236278,"version":"4.3.4"},"reference-count":73,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2018,3,30]],"date-time":"2018-03-30T00:00:00Z","timestamp":1522368000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/11\/110\/29248"],"award-info":[{"award-number":["PG\/11\/110\/29248"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["PG\/11\/80\/29135"],"award-info":[{"award-number":["PG\/11\/80\/29135"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2018,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Recent studies suggest that cardiac fibroblast\u2010specific p38\u03b1 MAPK contributes to the development of cardiac hypertrophy, but the underlying mechanism is unknown. Our study used a novel fibroblast\u2010specific, tamoxifen\u2010inducible p38\u03b1 knockout (KO) mouse line to characterize the role of fibroblast p38\u03b1 in modulating cardiac hypertrophy, and we elucidated the mechanism. Myocardial injury was induced in tamoxifen\u2010treated Cre\u2010positive p38\u03b1 KO mice or control littermates\n                    <jats:italic>via<\/jats:italic>\n                    chronic infusion of the \u03b2\u2010adrenergic receptor agonist isoproterenol. Cardiac function was assessed by pressure\u2010volume conductance catheter analysis and was evaluated for cardiac hypertrophy at tissue, cellular, and molecular levels. Isoproterenol infusion in control mice promoted overt cardiac hypertrophy and dysfunction (reduced ejection fraction, increased end systolic volume, increased cardiac weight index, increased cardiomyocyte area, increased fibrosis, and up\u2010regulation of myocyte fetal genes and hypertrophy\u2010associated microRNAs). Fibroblast\u2010specific p38\u03b1 KO mice exhibited marked protection against myocardial injury, with isoproterenol\u2010induced alterations in cardiac function, histology, and molecular markers all being attenuated. In\n                    <jats:italic>vitro<\/jats:italic>\n                    mechanistic studies determined that cardiac fibroblasts responded to damaged myocardium by secreting several paracrine factors known to induce cardiomyocyte hypertrophy, including IL\u20106, whose secretion was dependent upon p38\u03b1 activity. In conclusion, cardiac fibroblast p38\u03b1 contributes to cardiomyocyte hypertrophy and cardiac dysfunction, potentially\n                    <jats:italic>via<\/jats:italic>\n                    a mechanism involving paracrine fibroblast\u2010to\u2010myocyte IL\u20106 signaling.\u2014Bageghni, S.A., Hemmings, K.E., Zava, N., Denton, C. P., Porter, K. E., Ainscough, J. F. X., Drinkhill, M. J., Turner, N. A. Cardiac fibroblast\u2010specific p38\u03b1 MAP kinase promotes cardiac hypertrophy\n                    <jats:italic>via<\/jats:italic>\n                    a putative paracrine interleukin\u20106 signaling mechanism. FASEB J. 32, 4941\u20134954 (2018).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201701455rr","type":"journal-article","created":{"date-parts":[[2018,3,30]],"date-time":"2018-03-30T18:07:49Z","timestamp":1522433269000},"page":"4941-4954","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":68,"title":["Cardiac fibroblast\u2010specific p38\u03b1 MAP kinase promotes cardiac hypertrophy\n                    <i>via<\/i>\n                    a putative paracrine interleukin\u20106 signaling mechanism"],"prefix":"10.1096","volume":"32","author":[{"given":"Sumia A.","family":"Bageghni","sequence":"first","affiliation":[{"name":"Leeds Institute of Cardiovascular and Metabolic Medicine School of Medicine University of Leeds Leeds United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen E.","family":"Hemmings","sequence":"additional","affiliation":[{"name":"Leeds Institute of Cardiovascular and Metabolic Medicine School of Medicine University of Leeds Leeds United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ngonidzashe","family":"Zava","sequence":"additional","affiliation":[{"name":"Leeds Institute of Cardiovascular and Metabolic Medicine School of Medicine University of Leeds Leeds United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher P.","family":"Denton","sequence":"additional","affiliation":[{"name":"Centre for Rheumatology Division of Medicine University College London London United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen E.","family":"Porter","sequence":"additional","affiliation":[{"name":"Leeds Institute of Cardiovascular and Metabolic Medicine School of Medicine University of Leeds Leeds United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin F. 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