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Mice overexpressing transcription factor Fosl-2 (Fosl-2\n                    <jats:sup>tg<\/jats:sup>\n                    ) represent animal model of SSc. Fosl-2\n                    <jats:sup>tg<\/jats:sup>\n                    mice showed interstitial cardiac fibrosis, disorganized connexin-43\/40 in intercalated discs and deregulated expression of genes controlling conduction system, and developed higher heart rate (HR), prolonged QT intervals, arrhythmias with prevalence of premature ventricular contractions, ventricular tachycardias, II-degree atrio-ventricular blocks and reduced HR variability. Following stimulation with isoproterenol Fosl-2\n                    <jats:sup>tg<\/jats:sup>\n                    mice showed impaired HR response. In contrast to Fosl-2\n                    <jats:sup>tg<\/jats:sup>\n                    , immunodeficient Rag2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    Fosl-2\n                    <jats:sup>tg<\/jats:sup>\n                    mice were protected from enhanced myocardial fibrosis and ECG abnormalities. Transcriptomics analysis demonstrated that Fosl-2-overexpression was responsible for profibrotic signature of cardiac fibroblasts, whereas inflammatory component in Fosl-2\n                    <jats:sup>tg<\/jats:sup>\n                    mice activated their fibrotic and arrhythmogenic phenotype. In human cardiac fibroblasts FOSL-2-overexpression enhanced myofibroblast signature under proinflammatory or profibrotic stimuli. These results demonstrate that under immunofibrotic conditions transcription factor Fosl-2 exaggerates myocardial fibrosis, arrhythmias and aberrant response to stress.\n                  <\/jats:p>","DOI":"10.1038\/s42003-023-04534-6","type":"journal-article","created":{"date-parts":[[2023,2,9]],"date-time":"2023-02-09T05:10:20Z","timestamp":1675919420000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["The AP-1 transcription factor Fosl-2 drives cardiac fibrosis and arrhythmias under immunofibrotic conditions"],"prefix":"10.1038","volume":"6","author":[{"given":"Mara","family":"Stellato","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Dewenter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal","family":"Rudnik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amela","family":"Hukara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5620-4796","authenticated-orcid":false,"given":"\u00c7agla","family":"\u00d6zsoy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Renoux","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Pachera","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix","family":"Gantenbein","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"Seebeck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siim","family":"Uhtjaerv","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Osto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Razansky","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Klingel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joerg","family":"Henes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliver","family":"Distler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Przemys\u0142aw","family":"B\u0142yszczuk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3788-4594","authenticated-orcid":false,"given":"Gabriela","family":"Kania","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2023,2,9]]},"reference":[{"key":"4534_CR1","doi-asserted-by":"publisher","first-page":"705","DOI":"10.1038\/s41584-019-0322-7","volume":"15","author":"JHW Distler","year":"2019","unstructured":"Distler, J. 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Distler (2 years backwards, 2020-2022): Prof. O. Distler has\/had consultancy relationship with and\/or has received research funding from or has served as a speaker for the following companies in the area of potential treatments for systemic sclerosis and its complications in the last two years: 4P-Pharma, Abbvie, Acceleron, Alcimed, Altavant, Amgen, AnaMar, Arxx, AstraZeneca, Blade, Bayer, Boehringer Ingelheim, Corbus, CSL Behring, Galderma, Galapagos, Glenmark, Gossamer, iQvia, Kymera, Lupin, Medscape, Merck, Miltenyi Biotec, Mitsubishi Tanabe; Novartis, Prometheus, Redxpharna, Roivant, and Topadur in the area of potential treatments of scleroderma and its complications. Patent issued \u201cmir-29 for the treatment of systemic sclerosis\u201d (US8247389, EP2331143). Research Grants: Kymera, Mitsubishi. All other authors declare no competing interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"161"}}