Evidence map›Paper›PMID 39382090›Full record

ArticleJournal of cellular physiology2025

A combination of major histocompatibility complex (MHC) I overexpression and type I interferon induce mitochondrial dysfunction in human skeletal myoblasts.

Anastasia Thoma, Razan Alomosh, Holly L Bond, Tania Akter-Miah, Nasser Al-Shanti, Hans Degens, Vanja Pekovic-Vaughan, Adam P Lightfoot

Abstract read
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In one paragraph

Article in Journal of cellular physiology, 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. Review
  2. Article
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

8 authors.

Anastasia ThomaDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.
Razan AlomoshDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.
Holly L BondDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.
Tania Akter-MiahDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.
Nasser Al-ShantiDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.ORCID 0000-0002-4215-2649
Hans DegensDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.
Vanja Pekovic-VaughanDepartment of Musculoskeletal and Ageing Science, Faculty of Health and Life Science, University of Liverpool, Liverpool, UK.
Adam P LightfootDepartment of Life Sciences, Faculty of Science & Engineering, Manchester Metropolitan University, Manchester, UK.ORCID 0000-0003-1501-7879

Funding

BBRSC UK BB/W010801/1BBRSC UK BB/W018314/1Biotechnology and Biological Sciences Research CouncilManchester Metropolitan UniversityMedical Research CouncilMRC UK MR/P003311/1MRC-VA UK as part of CIMA MR/P020941/1MRC-VA UK as part of CIMA MR/R502182/1Muscular Dystrophy UKPhysiological SocietyRosetrees TrustRoyal SocietyThe Royal Society RGS\R2\180028
6 · The paper itself

Abstract

The overexpression of major histocompatibility complex (MHC) I on the surface of muscle fibers is a characteristic hallmark of the idiopathic inflammatory myopathies (IIMs), collectively termed myositis. Alongside MHC-I overexpression, subtypes of myositis, display a distinct type I interferon (IFN) signature. This study examined the combinational effects of elevated MHC-I and type I IFNs (IFNα/β) on mitochondrial function, as mitochondrial dysfunction is often seen in IIMs. Human skeletal muscle myoblasts were transfected with an MHC-I isoform using the mammalian HLA-A2/K

Indexed as

Interferon Type IMembrane Potential, MitochondrialMyoblasts, SkeletalCell LineGlycolysisHistocompatibility Antigens Class IHumansInterferon-alphaInterferon-betaMitochondriaMyositisNitric OxideReactive Oxygen SpeciesHistocompatibility Antigens Class IInterferon-alphaInterferon-betaInterferon Type INitric OxideReactive Oxygen Speciesidiopathic inflammatory myopathiesmajor histocompatibility complex Imitochondriamyositisreactive and nitric oxygen speciestype I interferon

Identifiers

PMID39382090
PMCPMC11701868

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.