Evidence map›Paper›PMID 39890639›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025

A window into intracellular events in myositis through subcellular proteomics.

Jennifer M Peterson, Valérie Leclair, Olumide E Oyebode, Dema M Herzallah, Andrea L Nestor-Kalinoski, Jose Morais, René P Zahedi, Mazen Alamr, John A Di Battista, Marie Hudson

Abstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Jennifer M PetersonDepartment of Exercise and Rehabilitative Sciences, The University of Toledo, 2801 W. Bancroft St., MS 119, Toledo, OH, 43606, USA. jennifer.peterson@utoledo.edu.
Valérie LeclairDivision of Rheumatology, Department of Medicine, McGill University, Montreal, QC, Canada.
Olumide E OyebodeDepartment of Exercise and Rehabilitative Sciences, The University of Toledo, 2801 W. Bancroft St., MS 119, Toledo, OH, 43606, USA.
Dema M HerzallahDepartment of Exercise and Rehabilitative Sciences, The University of Toledo, 2801 W. Bancroft St., MS 119, Toledo, OH, 43606, USA.
Andrea L Nestor-KalinoskiDepartment of Surgery, Advanced Microscopy and Imaging Center, University of Toledo, Toledo, OH, USA.
Jose MoraisDivision of Geriatric Medicine and Research Institute, McGill University Health Centre, Montreal, QC, Canada.
René P ZahediSegal Cancer Proteomics Centre, Lady Davis Institute for Medical Research, Montreal, QC, Canada.
Mazen AlamrDepartment of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada.
John A Di BattistaDepartment of Medicine and Experimental Medicine, McGill University Health Centre Research Institute, Montreal, QC, Canada.
Marie HudsonDivision of Rheumatology, Department of Medicine, McGill University, Montreal, QC, Canada. marie.hudson@mcgill.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVE AND

designIdiopathic inflammatory myopathies (IIM) are a heterogeneous group of inflammatory muscle disorders of unknown etiology. It is postulated that mitochondrial dysfunction and protein aggregation in skeletal muscle contribute to myofiber degeneration. However, molecular pathways that lead to protein aggregation in skeletal muscle are not well defined. SUBJECTS: Here we have isolated membrane-bound organelles (e.g., nuclei, mitochondria, sarcoplasmic/endoplasmic reticulum, Golgi apparatus, and plasma membrane) from muscle biopsies of normal (n = 3) and muscle disease patients (n = 11). Of the myopathy group, 10 patients displayed mitochondrial abnormalities (IIM (n = 9); mitochondrial myopathy (n = 1)), and one IIM patient did not show mitochondrial abnormalities (polymyositis).

methodsGlobal proteomic analysis was performed using an Orbitrap Fusion mass spectrometer. Upon unsupervised clustering, normal and mitochondrial myopathy muscle samples clustered separately from IIM samples.

resultsWe have confirmed previously known protein alterations in IIM and identified several new ones. For example, we found differential expression of (i) nuclear proteins that control cell division, transcription, RNA regulation, and stability, (ii) ER and Golgi proteins involved in protein folding, degradation, and protein trafficking in the cytosol, and (iii) mitochondrial proteins involved in energy production/metabolism and alterations in cytoskeletal and contractile machinery of the muscle.

conclusionsOur data demonstrates that molecular alterations are not limited to protein aggregations in the cytosol (inclusions) and occur in nuclear, mitochondrial, and membrane compartments of IIM skeletal muscle.

Indexed as

Muscle, SkeletalMyositisAdultAgedFemaleHumansMaleMiddle AgedProteomicsBiopsyHumanMuscleMyositisProteomics

Identifiers

PMID39890639
PMCPMC11785624

What Socratic holds

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LicenceCC BY
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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 Socratic graph.