{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T23:01:14Z","timestamp":1791500474057,"version":"4.3.4"},"reference-count":37,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2009,3,16]],"date-time":"2009-03-16T00:00:00Z","timestamp":1237161600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["K08 NS049346"],"award-info":[{"award-number":["K08 NS049346"]}],"id":[{"id":"10.13039\/100000002","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":[[2009,8]]},"abstract":"<jats:p>\n                    Duchenne\u2010Meryon muscular dystrophy (DMD) is the most common and lethal genetic muscle disease. Ameliorating muscle necrosis, inflammation, and fibrosis represents an important therapeutic approach for DMD. Imatinib, an antineoplastic agent, demonstrated antiinflammatory and antifibrotic effects in liver, kidney, lung, and skin of various animal models. This study tested antiinflammatory and antifibrotic effects of imatinib in\n                    <jats:italic>mdx<\/jats:italic>\n                    mice, a DMD mouse model. We treated\n                    <jats:italic>mdx<\/jats:italic>\n                    mice with intraperitoneal injections of imatinib at the peak of limb muscle inflammation and the onset of diaphragm fibrosis. Controls received PBS vehicle or were left untreated. Muscle necrosis, inflammation, fibrosis, and function were evaluated by measuring serum CK activity, endomysial CD45 immunoreactive inflammation area, endomysial collagen III deposition, and hind limb grip strength. Phosphorylation of the tyrosine kinase targets of imatinib was assessed by Western blot in diaphragm tissue and in primary cultures of peritoneal macrophages and skeletal muscle fibroblasts. Imatinib markedly reduced muscle necrosis, inflammation, and fibrosis, and significantly improved hind limb grip strength in\n                    <jats:italic>mdx<\/jats:italic>\n                    mice. Reduced clinical disease was accompanied by inhibition of c\u2010abl and PDGFR phosphorylation and suppression of TNF\u2010\u03b1 and IL\u2010\u03b2 expression. Imatinib therapy for DMD may hold promise for ameliorating muscle necrosis, inflammation, and fibrosis by inhibiting c\u2010abl and PDGFR signaling pathways and downstream inflammatory cytokine and fibrotic gene expression.\u2014 Huang, P., Zhao, X. S., Fields, M., Ransohoff, R. M., Zhou, L. Imatinib attenuates skeletal muscle dystrophy in\n                    <jats:italic>mdx<\/jats:italic>\n                    mice. FASEBJ. 23, 2539\u20132548 (2009)\n                  <\/jats:p>","DOI":"10.1096\/fj.09-129833","type":"journal-article","created":{"date-parts":[[2009,3,16]],"date-time":"2009-03-16T21:21:52Z","timestamp":1237238512000},"page":"2539-2548","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":94,"title":["Imatinib attenuates skeletal muscle dystrophy in\n                    <i>mdx<\/i>\n                    mice"],"prefix":"10.1096","volume":"23","author":[{"given":"Ping","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Neurology Neurological Institute Neuroinflammation Research Center Department of Neurosciences Lerner Research Institute Cleveland Clinic Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinyu S.","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Neurology Neurological Institute Neuroinflammation Research Center Department of 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