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Cited by 424

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Histone deacetylase degradation andMEF2 activation promote the formation of slow-twitch myofibers

Open access
Potthoff, Matthew J., Wu, Hai, Arnold, Michael A., Shelton, John M., Backs, Johannes, McAnally, John, Richardson, James A., Bassel-Duby, Rhonda, Olson, Eric N.·2007·Journal of Clinical Investigation
DOI 10.1172/jci31960
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Abstract

Skeletal muscle is composed of heterogeneous myofibers with distinctive rates of contraction, metabolic properties, and susceptibility to fatigue. We show that class II histone deacetylase (HDAC) proteins, which function as transcriptional repressors of the myocyte enhancer factor 2 (MEF2) transcription factor, fail to accumulate in the soleus, a slow muscle, compared with fast muscles (e.g., white vastus lateralis). Accordingly, pharmacological blockade of proteasome function specifically increases expression of class II HDAC proteins in the soleus in vivo. Using gain- and loss-of-function approaches in mice, we discovered that class II HDAC proteins suppress the formation of slow twitch, oxidative myofibers through the repression of MEF2 activity. Conversely, expression of a hyperactive form of MEF2 in skeletal muscle of transgenic mice promotes the formation of slow fibers and enhances running endurance, enabling mice to run almost twice the distance of WT littermates. Thus, the selective degradation of class II HDACs in slow skeletal muscle provides a mechanism for enhancing physical performance and resistance to fatigue by augmenting the transcriptional activity of MEF2. These findings provide what we believe are new insights into the molecular basis of skeletal muscle function and have important implications for possible therapeutic interventions into muscular diseases.

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Metadata

Authors
Potthoff, M. J., Wu, H., Arnold, M. A., Shelton, J. M., Backs, J., McAnally, J., Richardson, J. A., Bassel-Duby, R., & Olson, E. N.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2007-09-04
Volume
117
Issue
9
Pages
2459-2467
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci31960
OpenAlex
W2126580445
Cited by
424
References
3
FWCI
8.26
Type
journal article
Language
en
Open access
bronze

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