ArticleThe Journal of clinical investigation2007
Two tales concerning skeletal muscle.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- L-Arginine Enhances Protein Synthesis by Phosphorylating mTOR (Thr 2446) in a Nitric Oxide-Dependent Manner in C2C12 Cells.Oxidative medicine and cellular longevity · 2018Article
- Increased Circulating Levels of Interleukin-6 Induce Perturbation in Redox-Regulated Signaling Cascades in Muscle of Dystrophic Mice.Oxidative medicine and cellular longevity · 2017Article
- Intense Resistance Exercise Promotes the Acute and Transient Nuclear Translocation of Small Ubiquitin-Related Modifier (SUMO)-1 in Human Myofibres.International journal of molecular sciences · 2016Article
- Inhibition of Stat3 activation suppresses caspase-3 and the ubiquitin-proteasome system, leading to preservation of muscle mass in cancer cachexia.The Journal of biological chemistry · 2015Article
- Functional and Morphological Improvement of Dystrophic Muscle by Interleukin 6 Receptor Blockade.EBioMedicine · 2015Article
- STAT3 activation in skeletal muscle links muscle wasting and the acute phase response in cancer cachexia.PloS one · 2011Article
- Article
Corrections and comments
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- Erratum issued
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.