Evidence map›Paper›PMID 35775116›Full record

ArticleJournal of cachexia, sarcopenia and muscle2022

Amelioration of inflammatory myopathies by glucagon-like peptide-1 receptor agonist via suppressing muscle fibre necroptosis.

Mari Kamiya, Fumitaka Mizoguchi, Shinsuke Yasuda

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  8. Review
  9. Targeting Sarcopenia in CKD: The Emerging Role of GLP-1 Receptor Agonists.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025
    Review
  14. Article
  15. The emerging roles of necroptosis in skeletal muscle health and disease.Pflugers Archiv : European journal of physiology · 2024
    Review
  16. Glucagon-like peptide-1 receptor: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024 · on this map
    Review
  17. Article
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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

3 authors at 1 institution in 1 country.

Mari KamiyaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0002-2093-3823
Fumitaka MizoguchiDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Shinsuke YasudaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0001-6171-2077
Tokyo Medical and Dental University · JP

Funding

ImmunoForgeJSPS KAKENHI JP19K23839JSPS KAKENHI JP20K17422
6 · The paper itself

Abstract

backgroundAs glucocorticoids induce muscle atrophy during the treatment course of polymyositis (PM), novel therapeutic strategy is awaited that suppresses muscle inflammation but retains muscle strength. We recently found that injured muscle fibres in PM undergo FASLG-mediated necroptosis, a form of regulated cell death accompanied by release of pro-inflammatory mediators, contributes to accelerate muscle inflammation and muscle weakness. Glucagon-like peptide-1 receptor (GLP-1R) agonists have pleiotropic actions including anti-inflammatory effects, prevention of muscle atrophy, and inhibition of cell death, in addition to anti-diabetic effect. We aimed in this study to examine the role of GLP-1R in PM and the effect of a GLP-1R agonist on in vivo and in vitro models of PM.

methodsMuscle specimens of PM patients and a murine model of PM, C protein-induced myositis (CIM), were examined for the expression of GLP-1R. The effect of PF1801, a GLP-1R agonist, on CIM was evaluated in monotherapy or in combination with prednisolone (PSL). As an in vitro model of PM, C2C12-derived myotubes were treated with FASLG to induce necroptosis. The effect of PF1801 on this model was analysed.

resultsGLP-1R was expressed on the inflamed muscle fibres of PM and CIM. The treatment of CIM with PF1801 in monotherapy (PF) or in combination with PSL (PF + PSL) suppressed CIM-induced muscle weakness (grip strength, mean ± SD (g); PF 227 ± 6.0 (P < 0.01), PF + PSL 224 ± 8.5 (P < 0.01), Vehicle 162 ± 6.0) and decrease in cross-sectional area of muscle fibres (mean ± SD (μm

conclusionsGLP-1R agonist could be a novel therapy for PM that recovers muscle weakness and suppresses muscle inflammation through inhi biting muscle fibre necroptosis.

Indexed as

Glucagon-Like Peptide-1 Receptor AgonistsMyositisNecroptosisAMP-Activated Protein KinasesAnimalsHumansInflammationInflammation MediatorsMiceMuscle Fibers, SkeletalMuscle WeaknessMuscular AtrophyAMP-Activated Protein KinasesGlucagon-Like Peptide-1 Receptor AgonistsInflammation MediatorsGLP-1R agonistInflammatory myopathiesNecroptosisOxidative stressPolymyositis

Identifiers

PMID35775116
PMCPMC9397554
OpenAlexW4283749339

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.