{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T03:26:36Z","timestamp":1789097196243,"version":"build-2803163510"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2017,11,1]],"date-time":"2017-11-01T00:00:00Z","timestamp":1509494400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Although p38 mitogen-activated protein kinase (MAPK) is known to have a role in ischemic heart disease and many other diseases, its contribution to the pathobiology of right ventricular (RV) hypertrophy and failure is unclear. Therefore, we sought to investigate the role of p38 MAPK in the pathophysiology of pressure overload\u2013induced RV hypertrophy and failure. The effects of the p38 MAPK inhibitor PH797804 were investigated in mice with RV hypertrophy\/failure caused by exposure to hypoxia or pulmonary artery banding. In addition, the effects of p38 MAPK inhibition or depletion (by small interfering RNA) were studied in isolated mouse RV fibroblasts. Echocardiography, invasive hemodynamic measurements, immunohistochemistry, collagen assays, immunofluorescence staining, and Western blotting were performed. Expression of phosphorylated p38 MAPK was markedly increased in mouse and human hypertrophied\/failed RVs. In mice, PH797804 improved RV function and inhibited cardiac fibrosis compared with placebo. In isolated RV fibroblasts, p38 MAPK inhibition reduced transforming growth factor (TGF)-\u03b2\u2013induced collagen production as well as stress fiber formation. Moreover, p38 MAPK inhibition\/depletion suppressed TGF-\u03b2\u2013induced SMAD2\/3 phosphorylation and myocardin-related transcription factor A (MRTF-A) nuclear translocation, and prevented TGF-\u03b2\u2013induced cardiac fibroblast transdifferentiation. Moreover, p38 MAPK inhibition in mice exposed to pulmonary artery banding led to diminished nuclear levels of MRTF-A and phosphorylated SMAD3 in RV fibroblasts. Together, our data indicate that p38 MAPK inhibition significantly improves RV function and inhibits RV fibrosis. Inhibition of p38 MAPK in RV cardiac fibroblasts, resulting in coordinated attenuation of MRTF-A cytoplasmic\u2013nuclear translocation and SMAD3 deactivation, indicates that p38 MAPK signaling contributes to distinct disease-causing mechanisms.<\/jats:p>","DOI":"10.1165\/rcmb.2016-0374oc","type":"journal-article","created":{"date-parts":[[2017,6,28]],"date-time":"2017-06-28T15:34:01Z","timestamp":1498664041000},"page":"603-614","source":"Crossref","is-referenced-by-count":93,"title":["p38 MAPK Inhibition Improves Heart Function in Pressure-Loaded Right Ventricular Hypertrophy"],"prefix":"10.1093","volume":"57","author":[{"given":"Baktybek","family":"Kojonazarov","sequence":"first","affiliation":[{"name":"Universities of Giessen and Marburg Lung Center, Excellence Cluster Cardio-Pulmonary System, Member of the German Center for Lung Research, Giessen, 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Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hossein A.","family":"Ghofrani","sequence":"additional","affiliation":[{"name":"Universities of Giessen and Marburg Lung Center, Excellence Cluster Cardio-Pulmonary System, Member of the German Center for Lung Research, Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norbert","family":"Weissmann","sequence":"additional","affiliation":[{"name":"Universities of Giessen and Marburg Lung Center, Excellence Cluster Cardio-Pulmonary System, Member of the German Center for Lung Research, Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harm J.","family":"Bogaard","sequence":"additional","affiliation":[{"name":"VU University Medical Center, Amsterdam, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Werner","family":"Seeger","sequence":"additional","affiliation":[{"name":"Universities of Giessen and Marburg Lung 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