Evidence map›Paper›PMID 32896253›Full record

ArticleClinical and experimental rheumatology

Accumulation of autophagosome cargo protein p62 is common in idiopathic inflammatory myopathies.

Jose C Milisenda, Iago Pinal-Fernandez, Thomas E Lloyd, Josep María Grau, Frederick W Miller, Albert Selva-O'Callaghan, Lisa Christopher-Stine, Werner Stenzel, Andrew L Mammen, Andrea M Corse

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental rheumatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Current biomarkers in inclusion body myositis.Journal of neuromuscular diseases · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023
    Article
  15. Article
  16. Idiopathic inflammatory myopathies.Nature reviews. Disease primers · 2021
    Review
  17. Idiopathic inflammatory myopathies.Nature reviews. Disease primers · 2021
    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

10 authors at 4 institutions in 2 countries.

Jose C MilisendaMuscle Research Unit, Internal Medicine Service, Hospital Clínic de Barcelona, Universidad de Barcelona and CIBERER, Barcelona, Spain.
Iago Pinal-FernandezMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulations, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; and Faculty of Computer Science, Multimedia and Telecommunications and Faculty of Health Sciences, Universitat Oberta de Catalunya, Barcelona, Spain.
Thomas E LloydDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Josep María GrauMuscle Research Unit, Internal Medicine Service, Hospital Clínic de Barcelona, Universidad de Barcelona and CIBERER, Barcelona, Spain.
Frederick W MillerEnviromental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD, USA.
Albert Selva-O'CallaghanVall d'Hebron Hospital and Autonomous University of Barcelona, Spain.
Lisa Christopher-StineDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Werner StenzelDepartments of Neurology and Neuropathology, Charité-Universitätsmedizin, Berlin, Germany.
Andrew L MammenMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulations, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; and Vall d'Hebron Hospital and Autonomous University of Barcelona, Spain.
Andrea M CorseDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. acorse@jhmi.edu.
Johns Hopkins Medicine · USUniversitat de Barcelona · ESJohns Hopkins University · USVall d'Hebron Hospital Universitari · ES

Funding

Environmental/genetic Risk Factors and Pathogenesis of Autoimmune DiseaseZIAES101074 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RIDER, LISA · 2009 to 2025
$34.6M
Muscle Disease UnitZIAAR041203 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MAMMEN, ANDREW · 2015 to 2025
$19.7M
Pathogenesis and treatment of sporadic Inclusion Body Myositis in mouse models.R01AR076390 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI LLOYD, THOMAS E., WONG, PHILIP C · 2020 to 2024
$2.2M
NIAMS NIH HHS R01 AR076390
6 · The paper itself

Abstract

objectivesThe subsarcolemmal accumulation of p62 aggregates in myofibres has been proposed to be characteristic of sporadic inclusion body myositis (sIBM). The objective of this study was to analyse the patterns and prevalence of p62 immunostaining and to quantitate p62 gene expression in muscle biopsies from a large number of patients with different types of myopathic and neurogenic disorders.

methodsFor the p62 immunostaining analysis, all patients with a muscle biopsy immunostained for p62 at the Johns Hopkins Neuromuscular Pathology Laboratory from 2013 to 2017 were included (n=303). The prevalence and pattern of p62 immunostaining were compared between patients with histologically normal muscle (n=29), inflammatory myopathies (n=136), non-inflammatory myopathies (n=53), and neurogenic disorders (n=85). p62 expression levels were analysed using an existing RNAseq dataset including data from dermatomyositis (DM; n=39), immune-mediated necrotising myopathy (IMNM; n=49), antisynthetase syndrome (AS; n=18), and sIBM (n=23) patients as well as 20 histologically normal muscle biopsies.

resultsp62 staining was absent in normal biopsies, but present in biopsies from those with polymyositis (29%), non-inflammatory myopathies (all <31%), neurogenic disorders (31%), dermatomyositis (57%), sIBM (92%) and IMNM (87%). In all diseases studied, p62 accumulation was more prevalent in biopsies with more severe muscle damage. sIBM biopsies had decreased p62 expression levels compared to the other groups (corrected p<0.04).

conclusionsp62 accumulation is a general response to muscle injury and not a specific marker for sIBM. Also, in sIBM, p62 RNA levels are decreased, suggesting that, in this disease, p62 aggregation is not due to overexpression.

Indexed as

Autoimmune DiseasesMyositisMyositis, Inclusion BodyPolymyositisAutophagosomesHumansMuscle, Skeletal

Identifiers

PMID32896253
PMCPMC9062971
OpenAlexW3083974603

What OpenQuestion holds

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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 OpenQuestion graph.