Evidence map›Paper›PMID 29735415›Full record

ArticleEBioMedicine2018

Interventions Targeting Glucocorticoid-Krüppel-like Factor 15-Branched-Chain Amino Acid Signaling Improve Disease Phenotypes in Spinal Muscular Atrophy Mice.

Lisa M Walter, Marc-Olivier Deguise, Katharina E Meijboom, Corinne A Betts, Nina Ahlskog, Tirsa L E van Westering, Gareth Hazell, Emily McFall, Anna Kordala, Suzan M Hammond and 11 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Effect ofInternational journal of molecular sciences · 2025
    Review
  6. Article
  7. KLF13 restrains Dll4-muscular Notch2 axis to improve the muscle atrophy.Journal of cachexia, sarcopenia and muscle · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Metabolic Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2021
    Review
  16. Revisiting the role of mitochondria in spinal muscular atrophy.Cellular and molecular life sciences : CMLS · 2021
    Review
  17. Spinal muscular atrophy: Broad disease spectrum and sex-specific phenotypes.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  18. Article
  19. Article
  20. Review
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

21 authors at 7 institutions in 4 countries.

Lisa M WalterInstitute of Neuroanatomy and Cell Biology, Hannover Medical School, Hannover, Germany; Center of Systems Neuroscience, Hannover, Germany.
Marc-Olivier DeguiseOttawa Hospital Research Institute, Regenerative Medicine Program, Ottawa, ON, Canada; Department of Medicine and Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
Katharina E MeijboomDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Corinne A BettsDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Nina AhlskogDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Tirsa L E van WesteringDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Gareth HazellDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Emily McFallOttawa Hospital Research Institute, Regenerative Medicine Program, Ottawa, ON, Canada; Department of Medicine and Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
Anna KordalaDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Suzan M HammondDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Frank AbendrothMedical Research Council, Laboratory of Molecular Biology, Cambridge, United Kingdom.
Lyndsay M MurrayEuan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom; Centre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
Hannah K ShorrockEuan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom; Centre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
Domenick A ProsdocimoCase Cardiovascular Research Institute, Case Western Reserve University School of Medicine, University Hospitals Case Medical Center, Cleveland, OH, USA.
Saptarsi M HaldarGladstone Institute of Cardiovascular Disease, San Francisco, CA, USA; Department of Medicine, Division of Cardiology University of California, San Francisco, CA, USA.
Mukesh K JainCase Cardiovascular Research Institute, Case Western Reserve University School of Medicine, University Hospitals Case Medical Center, Cleveland, OH, USA.
Thomas H GillingwaterEuan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Edinburgh, United Kingdom; Centre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
Peter ClausInstitute of Neuroanatomy and Cell Biology, Hannover Medical School, Hannover, Germany; Center of Systems Neuroscience, Hannover, Germany.
Rashmi KotharyOttawa Hospital Research Institute, Regenerative Medicine Program, Ottawa, ON, Canada; Department of Medicine and Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
Matthew J A WoodDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Melissa BowermanDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom. Electronic address: m.bowerman@keele.ac.uk.
University of Oxford · GBMott MacDonald (United Kingdom) · GBUniversity of Ottawa · CAMedizinische Hochschule Hannover · DEUniversity Hospitals Cleveland Medical Center · USGladstone Institutes · USMRC Laboratory of Molecular Biology · GB

Funding

Medical Research Council MC_U105178803Medical Research Council MR/L013142/1
6 · The paper itself

Abstract

The circadian glucocorticoid-Krüppel-like factor 15-branched-chain amino acid (GC-KLF15-BCAA) signaling pathway is a key regulatory axis in muscle, whose imbalance has wide-reaching effects on metabolic homeostasis. Spinal muscular atrophy (SMA) is a neuromuscular disorder also characterized by intrinsic muscle pathologies, metabolic abnormalities and disrupted sleep patterns, which can influence or be influenced by circadian regulatory networks that control behavioral and metabolic rhythms. We therefore set out to investigate the contribution of the GC-KLF15-BCAA pathway in SMA pathophysiology of Taiwanese Smn

Indexed as

Dietary SupplementsDNA-Binding ProteinsMuscular Atrophy, SpinalTranscription FactorsAmino Acids, Branched-ChainAnimalsDisease Models, AnimalKruppel-Like Transcription FactorsMiceMice, KnockoutPrednisoloneSignal TransductionAmino Acids, Branched-ChainDNA-Binding ProteinsKlf15 protein, mouseKruppel-Like Transcription FactorsPrednisoloneTranscription FactorsBranched-chain amino acidsGlucocorticoidsKLF15MetabolismSpinal muscular atrophyTherapy

Identifiers

PMID29735415
PMCPMC6013932
OpenAlexW2802576154

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.