Evidence map›Paper›PMID 34426497›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Identification of a KLF5-dependent program and drug development for skeletal muscle atrophy.

Lin Liu, Hiroyuki Koike, Takehito Ono, Shinichiro Hayashi, Fujimi Kudo, Atsushi Kaneda, Hiroyuki Kagechika, Ichiro Manabe, Tomoki Nakashima, Yumiko Oishi

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Lambertianic Acid fromPlants (Basel, Switzerland) · 2025
    Article
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  10. Review
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  12. KLF13 restrains Dll4-muscular Notch2 axis to improve the muscle atrophy.Journal of cachexia, sarcopenia and muscle · 2024
    Article
  13. Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024
    Review
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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.

Lin LiuDepartment of Biochemistry & Molecular Biology, Nippon Medical School, Tokyo 113-8602, Japan.ORCID 0000-0003-2278-964X
Hiroyuki KoikeDepartment of Biochemistry & Molecular Biology, Nippon Medical School, Tokyo 113-8602, Japan.ORCID 0000-0001-9934-6930
Takehito OnoDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.ORCID 0000-0003-2445-4253
Shinichiro HayashiDepartment of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8551, Japan.
Fujimi KudoDepartment of Systems Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0002-6980-5515
Hiroyuki KagechikaInstitute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Tokyo 101-0062, Japan.
Ichiro ManabeDepartment of Systems Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0001-9481-6673
Tomoki NakashimaDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.ORCID 0000-0001-6779-8617
Yumiko OishiDepartment of Biochemistry & Molecular Biology, Nippon Medical School, Tokyo 113-8602, Japan; yuooishi@gmail.com.ORCID 0000-0002-4761-0952

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle atrophy is caused by various conditions, including aging, disuse related to a sedentary lifestyle and lack of physical activity, and cachexia. Our insufficient understanding of the molecular mechanism underlying muscle atrophy limits the targets for the development of effective pharmacologic treatments and preventions. Here, we identified Krüppel-like factor 5 (KLF5), a zinc-finger transcription factor, as a key mediator of the early muscle atrophy program. KLF5 was up-regulated in atrophying myotubes as an early response to dexamethasone or simulated microgravity in vitro. Skeletal muscle-selective deletion of

Indexed as

Drug DevelopmentAnimalsBenzoatesDexamethasoneGene Expression RegulationGlucocorticoidsKruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLMice, KnockoutMuscle ProteinsMuscle, SkeletalMuscular AtrophySignal TransductionSKP Cullin F-Box Protein LigasesBenzoatesDexamethasoneFbxo32 protein, mouseGlucocorticoidsKlf5 protein, mouseKruppel-Like Transcription FactorsMuscle ProteinsSKP Cullin F-Box Protein LigasestamibaroteneTetrahydronaphthalenesTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesKLFmuscle atrophyRAR ligand

Identifiers

PMID34426497
PMCPMC8536343

What OpenQuestion holds

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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.