Evidence map›Paper›PMID 21824387›Full record

ArticleSkeletal muscle2011

Regulation of DMD pathology by an ankyrin-encoded miRNA.

Matthew S Alexander, Juan Carlos Casar, Norio Motohashi, Jennifer A Myers, Iris Eisenberg, Robert T Gonzalez, Elicia A Estrella, Peter B Kang, Genri Kawahara, Louis M Kunkel

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
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  6. Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025
    Review
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  19. miRNA-486-5p: signaling targets and role in non-malignant disease.Cellular and molecular life sciences : CMLS · 2022
    Review
  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Matthew S AlexanderProgram in Genomics and Division of Genetics, Children's Hospital Boston, 3 Blackfan Circle, CLS15024, Boston, MA 02115, USA. kunkel@enders.tch.havard.edu.
Juan Carlos Casar
Norio Motohashi
Jennifer A Myers
Iris Eisenberg
Robert T Gonzalez
Elicia A Estrella
Peter B Kang
Genri Kawahara
Louis M Kunkel
Boston Children's Hospital · USHarvard University · US

Funding

Progenitor Cells inHuman Skeletal MuscleP50NS040828 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI KOHANE, ISAAC S. · 2008 to 2011
$5.9M
NINDS NIH HHS P50 NS040828
6 · The paper itself

Abstract

backgroundDuchenne muscular dystrophy (DMD) is an X-linked myopathy resulting from the production of a nonfunctional dystrophin protein. MicroRNA (miRNA) are small 21- to 24-nucleotide RNA that can regulate both individual genes and entire cell signaling pathways. Previously, we identified several mRNA, both muscle-enriched and inflammation-induced, that are dysregulated in the skeletal muscles of DMD patients. One particularly muscle-enriched miRNA, miR-486, is significantly downregulated in dystrophin-deficient mouse and human skeletal muscles. miR-486 is embedded within the ANKYRIN1(ANK1) gene locus, which is transcribed as either a long (erythroid-enriched) or a short (heart muscle- and skeletal muscle-enriched) isoform, depending on the cell and tissue types.

resultsInhibition of miR-486 in normal muscle myoblasts results in inhibited migration and failure to repair a wound in primary myoblast cell cultures. Conversely, overexpression of miR-486 in primary myoblast cell cultures results in increased proliferation with no changes in cellular apoptosis. Using bioinformatics and miRNA reporter assays, we have identified platelet-derived growth factor receptor β, along with several other downstream targets of the phosphatase and tensin homolog deleted on chromosome 10/AKT (PTEN/AKT) pathway, as being modulated by miR-486. The generation of muscle-specific transgenic mice that overexpress miR-486 revealed that miR-486 alters the cell cycle kinetics of regenerated myofibers in vivo, as these mice had impaired muscle regeneration.

conclusionsThese studies demonstrate a link for miR-486 as a regulator of the PTEN/AKT pathway in dystrophin-deficient muscle and an important factor in the regulation of DMD muscle pathology.

Identifiers

PMID21824387
PMCPMC3188430
OpenAlexW2089528462

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.