Evidence map›Paper›PMID 39162115›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2025

Muscle Tissue Transcriptome of Idiopathic Inflammatory Myopathy Reflects the Muscle Damage Process by Monocytes and Presence of Skin Lesions.

Shinji Izuka, Natsuka Umezawa, Toshihiko Komai, Yusuke Sugimori, Naoki Kimura, Fumitaka Mizoguchi, Yuichiro Fujieda, Keita Ninagawa, Takeshi Iwasaki, Katsuya Suzuki and 12 more

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. 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

22 authors.

Shinji IzukaDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-9724-4911
Natsuka UmezawaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Toshihiko KomaiDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yusuke SugimoriDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Naoki KimuraDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Fumitaka MizoguchiDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Yuichiro FujiedaDepartment of Rheumatology, Endocrinology and Nephrology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-4705-341X
Keita NinagawaDepartment of Rheumatology, Endocrinology and Nephrology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0001-8082-1009
Takeshi IwasakiDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Katsuya SuzukiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0003-1111-8218
Koichiro OhmuraDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Tsuneyo MimoriDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Tatsuya AtsumiDepartment of Rheumatology, Endocrinology and Nephrology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Eiryo KawakamiCenter for Integrative Medical Sciences, the Institute of Physical and Chemical Research (RIKEN), Yokohama City, Kanagawa, Japan.
Akari SuzukiCenter for Integrative Medical Sciences, the Institute of Physical and Chemical Research (RIKEN), Yokohama City, Kanagawa, Japan.
Yuta KochiCenter for Integrative Medical Sciences, the Institute of Physical and Chemical Research (RIKEN), Yokohama City, Kanagawa, Japan.
Kazuhiko YamamotoDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, 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
Tomohisa OkamuraDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Mineto OtaDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Keishi FujioDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-7276-5254

Funding

The Japan Agency for Medical Research and Development (AMED) 19ek0410047
6 · The paper itself

Abstract

objectiveWe aim to investigate transcriptomic and immunophenotypic features of muscle specimens from patients with idiopathic inflammatory myopathy (IIM).

methodsBulk RNA-sequencing was performed on muscle biopsy samples from 16 patients with dermatomyositis (DM) and 9 patients with polymyositis (PM). Seven tested positive for anti-aminoacyl transfer RNA synthetase antibodies in the patients with DM (ARS-DM). We conducted weighted gene coexpression network analysis (WGCNA), differentially expressed gene (DEG) analysis, and gene set variation analysis to assess contributions of specific pathways. Cell proportions in muscle specimens were estimated using a deconvolution approach.

resultsWGCNA revealed significant positive correlations between serum creatine kinase (CK) levels and gene modules involved in cellular respiration, phagocytosis, and oxidative phosphorylation (OXPHOS). Significant positive correlations were also observed between CK levels and proportions of CD16-positive and negative monocytes and myeloid dendritic cells. Notably, patients with DM demonstrated enrichment of complement and interferon-α and γ pathway genes compared with those with PM. Furthermore, ARS-DM demonstrated a higher proportion of Th1 cells and DEGs related to OXPHOS. Additionally, serum Krebs von den Lungen-6 levels correlated with gene modules associated with extracellular matrix and the transforming growth factor-β signaling pathway.

conclusionOur study highlights a significant involvement of monocytes in muscle damage and delineates pathologic differences among IIM subtypes. DM was characterized by complement and interferon-α and γ signaling, whereas ARS-DM was associated with OXPHOS. Distinctive gene expression variations in muscle specimens suggest that different pathologic mechanisms underlie muscle damage in each IIM phenotype.

Indexed as

DermatomyositisMonocytesMuscle, SkeletalPolymyositisTranscriptomeAdultAgedBiopsyCreatine KinaseFemaleHumansMaleMiddle AgedMyositisOxidative PhosphorylationSkinCreatine Kinase

Identifiers

PMID39162115
PMCPMC11685001

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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.