{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T13:37:00Z","timestamp":1790257020865,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2008,10,14]],"date-time":"2008-10-14T00:00:00Z","timestamp":1223942400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:p>Contraction\u2010mediated injury is a major contributing factor to the pathophysiology of muscular dystrophy and therefore therapies that can attenuate this type of injury have clinical relevance. Systemic administration of insulin\u2010like growth factor\u2010I (IGF\u2010I) has been shown to improve muscle function in dystrophic <jats:italic>mdx<\/jats:italic> mice, an effect associated with a shift towards a more oxidative muscle phenotype and a reduced susceptibility to contraction\u2010mediated damage. The actions of IGF\u2010I <jats:italic>in vivo<\/jats:italic> are modulated by IGF binding proteins (IGFBPs), which generally act to inhibit IGF\u2010I signalling. We tested the hypothesis that an analogue of IGF\u2010I (LR IGF\u2010I), which has significantly reduced binding affinity for IGFBPs, would improve the dystrophic pathology by reducing the susceptibility to muscle injury. Dystrophic <jats:italic>mdx<\/jats:italic> and wild\u2010type (C57BL\/10) mice were administered LR IGF\u2010I continuously (\u223c1.5 mg kg<jats:sup>\u22121<\/jats:sup> day<jats:sup>\u22121<\/jats:sup>) via osmotic mini\u2010pump for 4 weeks. Administration of LR IGF\u2010I reduced the susceptibility of extensor digitorum longus, soleus and diaphragm muscles to contraction damage, as evident from lower force deficits after a protocol of lengthening contractions. In contrast to the mechanism of protection conferred by administration of IGF\u2010I, the protection conferred by LR IGF\u2010I was independent of changes in muscle fatigue and oxidative metabolism. This study further indicates that modulation of IGF\u2010I signalling has therapeutic potential for muscular diseases.<\/jats:p>","DOI":"10.1113\/expphysiol.2008.042838","type":"journal-article","created":{"date-parts":[[2008,6,21]],"date-time":"2008-06-21T00:25:20Z","timestamp":1214007920000},"page":"1190-1198","source":"Crossref","is-referenced-by-count":42,"title":["Insulin\u2010like growth factor\u2010I analogue protects muscles of dystrophic <i>mdx<\/i> mice from contraction\u2010mediated damage"],"prefix":"10.1113","volume":"93","author":[{"given":"Stefan M.","family":"Gehrig","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Ryall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan D.","family":"Schertzer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gordon 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