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Corrigendum Free access | 10.1172/JCI33379C1

Two tales concerning skeletal muscle

David J. Glass

Find articles by Glass, D. in: JCI | PubMed | Google Scholar

Published February 1, 2008 - More info

Published in Volume 118, Issue 2 on February 1, 2008
J Clin Invest. 2008;118(2):820–820. https://doi.org/10.1172/JCI33379C1.
© 2008 The American Society for Clinical Investigation
Published February 1, 2008 - Version history
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Two tales concerning skeletal muscle
David J. Glass
David J. Glass
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Two tales concerning skeletal muscle

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Abstract

It was previously appreciated that the determination of skeletal muscle fiber type (fast or slow) could be regulated by class II histone deacetylases (HDACs), which function by inhibiting the transcription factor myocyte enhancer factor 2 (MEF2). In a report by Potthoff et al. in this issue of the JCI, it is further shown that HDACs are degraded via the ubiquitin/proteasome pathway, opening up a search for the putative E3 ligase that mediates the proteolysis of the responsible HDACs (see the related article beginning on page 2459). In a second report, by Suzuki et al., a new convergence between the biology of muscular dystrophy and muscle atrophy is elucidated (see the related study beginning on page 2468). It had previously been known that NO signaling is dysregulated during muscular dystrophy due to the disruption of the dystrophin glycoprotein complex (DGC), which anchors neuronal NOS (nNOS). Here it is shown that nNOS is similarly perturbed in a setting of skeletal muscle atrophy. Both of these studies suggest new avenues for the treatment of skeletal muscle disease.

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David J. Glass

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Original citation: J. Clin. Invest. 117:2388-2391 (2007). doi:10.1172/JCI33379.

Citation for this corrigendum: J. Clin. Invest. 118:820 (2008). doi:10.1172/JCI33379C1.

The author wishes to revise the penultimate sentence of this article (page 2390) for clarity.

The corrected sentence appears below.

More immediately, a strategy to inhibit the dysregulation of nNOS activity in skeletal muscle may be beneficial.

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