Evidence map›Paper›PMID 20007902›Full record

ArticleScience (New York, N.Y.)2009

MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice.

Andrew H Williams, Gregorio Valdez, Viviana Moresi, Xiaoxia Qi, John McAnally, Jeffrey L Elliott, Rhonda Bassel-Duby, Joshua R Sanes, Eric N Olson

Abstract read
In one paragraph

Article in Science (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 440 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
440citing papers in PubMed, 2 pooled it
31.7field-weighted citation impact, top 1% 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

440 citing papers in PubMed, 2 syntheses or guidelines pooled it, 732 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Systemic brain-body metabolic coupling patterns in amyotrophic lateral sclerosis: a whole-body [European journal of nuclear medicine and molecular imaging · 2026
    Article
  12. Article
  13. Article
  14. Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. MicroRNAs in neurodegenerative diseases: from molecular mechanisms to clinical biomarkers, detection methods and therapeutic strategies-advances and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Andrew H WilliamsDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Gregorio Valdez
Viviana Moresi
Xiaoxia Qi
John McAnally
Jeffrey L Elliott
Rhonda Bassel-Duby
Joshua R Sanes
Eric N Olson
The University of Texas Southwestern Medical Center · USHarvard University · US

Funding

TRAINING IN CARDIOVASCULAR RESEARCHT32HL007360 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 1985 to 2012
$11.8M
MicroRNA Control of Cardiac Gene Expression, Function and DiseaseR01HL093039 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 2009 to 2013
$2.8M
UT Southwestern Small Animal Imaging ResourceU24CA126608 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MASON, RALPH P., SHERRY, DEAN · 2007 to 2011
$2.3M
Molecular basis of age-related synaptic alterationsF32NS061464 · NINDS · HARVARD UNIVERSITY · PI VALDEZ, GREGORIO · 2008 to 2010
$159k
NCI NIH HHS U24 CA126608NHLBI NIH HHS R01 HL093039NHLBI NIH HHS T32HL007360NINDS NIH HHS 1F32NS061464-01A1
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons, denervation of target muscles, muscle atrophy, and paralysis. Understanding ALS pathogenesis may require a fuller understanding of the bidirectional signaling between motor neurons and skeletal muscle fibers at neuromuscular synapses. Here, we show that a key regulator of this signaling is miR-206, a skeletal muscle-specific microRNA that is dramatically induced in a mouse model of ALS. Mice that are genetically deficient in miR-206 form normal neuromuscular synapses during development, but deficiency of miR-206 in the ALS mouse model accelerates disease progression. miR-206 is required for efficient regeneration of neuromuscular synapses after acute nerve injury, which probably accounts for its salutary effects in ALS. miR-206 mediates these effects at least in part through histone deacetylase 4 and fibroblast growth factor signaling pathways. Thus, miR-206 slows ALS progression by sensing motor neuron injury and promoting the compensatory regeneration of neuromuscular synapses.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAxonsCarrier ProteinsDisease Models, AnimalDisease ProgressionFibroblast Growth FactorsHistone DeacetylasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsMiceMice, TransgenicMicroRNAsMotor NeuronsMuscle DenervationMuscle, SkeletalCarrier ProteinsFgfbp1 protein, mouseFibroblast Growth FactorsHdac5 protein, mouseHistone DeacetylasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsMicroRNAsMirn206 microRNA, mouseMyoD1 myogenic differentiation proteinMyoD ProteinMyogenin

Identifiers

PMID20007902
PMCPMC2796560
OpenAlexW2125093810

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.