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Although there is currently no cure, one promising treatment for DMD is aimed at increasing endogenous levels of utrophin A to compensate functionally for the lack of dystrophin. Recent studies from our laboratory revealed that heparin treatment of mdx mice activates p38 MAPK, leading to an upregulation of utrophin A expression and improvements in the dystrophic phenotype. Based on these findings, we sought to determine the effects of other potent p38 activators, including the cyclooxygenase (COX)\u20102 inhibitor celecoxib. In this study, we treated 6\u2010wk\u2010old mdx mice for 4 wk with celecoxib. Immunofluorescence analysis of celecoxib\u2010treated mdx muscles revealed a fiber type switch from a fast to a slower phenotype along with beneficial effects on muscle fiber integrity. In agreement, celecoxib\u2010treated mdx mice showed improved muscle strength. Celecoxib treatment also induced increases in utrophin A expression ranging from ~1.5\u2010 to 2\u2010fold in tibialis anterior diaphragm and heart muscles. Overall, these results highlight that activation of p38 in muscles can indeed lead to an attenuation of the dystrophic phenotype and reveal the potential role of celecoxib as a novel therapeutic agent for the treatment of DMD.\u2014P\u00e9ladeau, C., Adam, N. J., Jasmin, B. J. Celecoxib treatment improves muscle function in mdx mice and increases utrophin A expression. 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