ArticleHeliyon2020
Investigating genetic drivers of dermatomyositis pathogenesis using meta-analysis.
Article in Heliyon, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- A comprehensive review of the emerging role of NRF3 in ovarian cancer tumorigenesis and progression.Journal of ovarian research · 2026Review
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Malignancy in Idiopathic Inflammatory Myopathies: Recent Insights.Clinical reviews in allergy & immunology · 2025Review
- Article
- Construction and validation of a diagnostic model for dermatomyositis based on the LASSO algorithm.Central-European journal of immunology · 2025Article
- Genetic Variant Analyses Identify Novel Candidate Autism Risk Genes from a Highly Consanguineous Cohort of 104 Families from Oman.International journal of molecular sciences · 2024Article
- Neutrophil and mononuclear leukocyte pathways and upstream regulators revealed by serum proteomics of adult and juvenile dermatomyositis.Arthritis research & therapy · 2024Article
- TRIM38 suppresses migration, invasion, metastasis, and proliferation in non-small cell lung cancer (NSCLC) via regulating the AMPK/NF-κB/NLRP3 pathway.Molecular and cellular biochemistry · 2024Article
- Amyopathic dermatomyositis may be on the spectrum of autoinflammatory disease: A clinical review.Rheumatology and immunology research · 2024Review
- Association of ZC3HAV1 single nucleotide polymorphisms with the susceptibility of Vogt-Koyanagi-Harada Disease.BMC medical genomics · 2023Article
- Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Review
- The molecular mechanism underlying dermatomyositis related interstitial lung disease: evidence from bioinformatic analysis andFrontiers in immunology · 2023Article
- Tripartite motif protein 6 promotes hepatocellular carcinoma progression via multiple pathways.Turkish journal of medical sciences · 2023Article
- A novel model of dermatomyositis induced by membrane antigen and calciphylaxis in rats.Biomedical reports · 2022Article
- Autophagy-related genes are potential diagnostic biomarkers for dermatomyositis.Annals of translational medicine · 2022Article
- Identification of Vital Hub Genes and Potential Molecular Pathways of Dermatomyositis by Bioinformatics Analysis.BioMed research international · 2021Article
- Emerging Roles of MHC Class I Region-Encoded E3 Ubiquitin Ligases in Innate Immunity.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
18 authors at 10 institutions in 1 country.
Funding
Abstract
aimsDermatomyositis (DM) is a progressive, idiopathic inflammatory myopathy with poorly understood pathogenesis. A hallmark of DM is an increased risk for developing breast, ovarian, and lung cancer. Since autoantibodies against anti-TIF-1-γ, a member of the tripartite motif (TRIM) proteins, has a strong association with malignancy, we examined expression of the TRIM gene family to identify pathways that may be contributing to DM pathogenesis. MATERIALS AND
methodsWe employed the Search Tag Analyze Resource for GEO platform to search the NCBI Gene Expression Omnibus to elucidate TRIM family gene expression as well as oncogenic drivers in DM pathology. We conducted meta-analysis of the data from human skin (60 DM vs 34 healthy) and muscle (71 DM vs 22 healthy). KEY
findingsWe identified genes involved in innate immunity, antigen presentation, metabolism, and other cellular processes as facilitators of DM disease activity and confirmed previous observations regarding the presence of a robust interferon signature. Moreover, analysis of DM muscle samples revealed upregulation of TRIM14, TRIM22, TRIM25, TRIM27, and TRIM38. Likewise, analysis of DM skin samples showed upregulation of TRIM5, TRIM6, TRIM 14, TRIM21, TRIM34, and TRIM38 and downregulation of TRIM73. Additionally, we noted upregulation of oncogenes IGLC1, IFI44, POSTN, MYC, NPM1, and IDO1 and related this change to interferon signaling. While the clinical data associated with genetic data that was analyzed did not contain clinical data regarding malignancy in these cohorts, the observed genetic changes may be associated with homeostatic and signaling changes that relate to the increased risk in malignancy in DM. SIGNIFICANCE: Our results implicate previously unknown genes as potential drivers of DM pathology and suggest certain TRIM family members may have disease-specific roles with potential diagnostic and therapeutic implications.
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