期刊
GENES & DEVELOPMENT
卷 28, 期 8, 页码 809-811出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.241182.114
关键词
SWI/SNF chromatin remodeling; BAF60; microRNA; HDAC; FAPs; muscular dystrophy
资金
- Association Francaise contre les Myopathies
- Canadian Institutes of Health Research
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.
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