title: Dystrophic muscle environment induces changes in cell plasticity.
abstract: Fibro-adipogenic progenitors (FAPs) reside in the muscle, where they facilitate myofiber regeneration. Under normal conditions, FAPs lack myogenic potential and thus do not directly contribute to regenerated myofibers. Surprisingly, Saccone and colleagues (pp. 841-857) demonstrated that the dystrophic muscle environment causes FAPs to adopt a chromatin state that imparts these cells with myogenic potential. In this context, treatment of muscle with deacetylase inhibitors activates a BAF60c-myomiR transcriptional network in FAPs, blocking adipogenesis and driving muscle differentiation.
authors.affiliation: Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario K1H 8L6, Canada;
authors.forename: Herve
authors.initials: H
authors.lastname: Faralli
authors.forename: F Jeffrey
authors.initials: FJ
authors.lastname: Dilworth
mesh_terms: D000818:Animals; D006655:Histone Deacetylases / Q000378:metabolism*; D035683:MicroRNAs / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000502:physiology*; D009136:Muscular Dystrophies / Q000235:genetics* / Q000503:physiopathology*; D013234:Stem Cells / Q000378:metabolism*
chemical_list: D035683:MicroRNAs; D006655:Histone Deacetylases
keywords: BAF60; FAPs; HDAC; SWI/SNF chromatin remodeling; microRNA; muscular dystrophy
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