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• W2095917282 abstract "Duchenne muscular dystrophy (DMD) is caused by the absence of dystrophin along muscle fibers. An attractive therapeutic avenue for DMD consists in the upregulation of utrophin A, a protein with high sequence identity and functional redundancy with dystrophin. Recent work has shown that pharmacological interventions that induce a muscle fiber shift toward a slower, more oxidative phenotype with increased expression of utrophin A confer morphological and functional improvements in mdx mice. Whether such improvements result from the increased expression of utrophin A per se or are linked to other beneficial adaptations associated with the slow, oxidative phenotype remain to be established. To address this central issue, we capitalized on the use of double knockout (dKO) mice, which are mdx mice also deficient in utrophin. We first compared expression of signaling molecules and markers of the slow, oxidative phenotype in muscles of mdx versus dKO mice and found that both strains exhibit similar phenotypes. Chronic activation of 5′ adenosine monophosphate-activated protein kinase with 5-amino-4-imidazolecarboxamide riboside (AICAR) resulted in expression of a slower, more oxidative phenotype in both mdx and dKO mice. In mdx mice, this fiber type shift was accompanied by clear functional improvements that included reductions in central nucleation, IgM sarcoplasmic penetration and sarcolemmal damage resulting from eccentric contractions, as well as in increased grip strength. These important morphological and functional adaptations were not seen in AICAR-treated dKO mice. Our findings show the central role of utrophin A in mediating the functional benefits associated with expression of a slower, more oxidative phenotype in dystrophic animals." @default.
• W2095917282 created "2016-06-24" @default.
• W2095917282 creator A5008505811 @default.
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• W2095917282 date "2014-10-16" @default.
• W2095917282 modified "2023-10-01" @default.
• W2095917282 title "Utrophin A is essential in mediating the functional adaptations of mdx mouse muscle following chronic AMPK activation" @default.
• W2095917282 cites W1492569783 @default.
• W2095917282 cites W1584198130 @default.
• W2095917282 cites W1585410256 @default.
• W2095917282 cites W1963965557 @default.
• W2095917282 cites W1967886094 @default.
• W2095917282 cites W1968210959 @default.
• W2095917282 cites W1972387026 @default.
• W2095917282 cites W1985130783 @default.
• W2095917282 cites W1989317478 @default.
• W2095917282 cites W1989689747 @default.
• W2095917282 cites W1999008715 @default.
• W2095917282 cites W1999243649 @default.
• W2095917282 cites W2001548627 @default.
• W2095917282 cites W2004909768 @default.
• W2095917282 cites W2007914493 @default.
• W2095917282 cites W2013060005 @default.
• W2095917282 cites W2026728314 @default.
• W2095917282 cites W2036132575 @default.
• W2095917282 cites W2041946214 @default.
• W2095917282 cites W2042996461 @default.
• W2095917282 cites W2047015778 @default.
• W2095917282 cites W2053765200 @default.
• W2095917282 cites W2054963293 @default.
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• W2095917282 cites W2062746471 @default.
• W2095917282 cites W2073377967 @default.
• W2095917282 cites W2074781910 @default.
• W2095917282 cites W2078680005 @default.
• W2095917282 cites W2080417224 @default.
• W2095917282 cites W2087864381 @default.
• W2095917282 cites W2091212285 @default.
• W2095917282 cites W2095118539 @default.
• W2095917282 cites W2098016509 @default.
• W2095917282 cites W2102878417 @default.
• W2095917282 cites W2106898598 @default.
• W2095917282 cites W2107945166 @default.
• W2095917282 cites W2112943033 @default.
• W2095917282 cites W2113931353 @default.
• W2095917282 cites W2114349736 @default.
• W2095917282 cites W2117978515 @default.
• W2095917282 cites W2120747625 @default.
• W2095917282 cites W2121823236 @default.
• W2095917282 cites W2121907426 @default.
• W2095917282 cites W2124434598 @default.
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• W2095917282 cites W2129216549 @default.
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• W2095917282 cites W2149091819 @default.
• W2095917282 cites W2150377102 @default.
• W2095917282 cites W2151700620 @default.
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• W2095917282 cites W2159443359 @default.
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• W2095917282 cites W2164533103 @default.
• W2095917282 cites W2166810075 @default.
• W2095917282 cites W2169836157 @default.
• W2095917282 cites W2176414067 @default.
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• W2095917282 doi "https://doi.org/10.1093/hmg/ddu535" @default.
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• W2095917282 hasPublicationYear "2014" @default.
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