ArticleFrontiers in immunology2022
Identifying hub circadian rhythm biomarkers and immune cell infiltration in rheumatoid arthritis.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of potential key efferocytosis-related genes in rheumatoid arthritis using machine learning.Clinical rheumatology · 2026Article
- Global burden and trends of rheumatoid arthritis attributable to smoking from 1990 to 2021 with forecasts to 2050.Tropical medicine and health · 2026Article
- Identification and Experimental Validation of Key Biomarkers for Rheumatoid Arthritis Based on Bioinformatics Analysis and Machine Learning.Journal of inflammation research · 2026Article
- The role of circadian rhythm regulator PERs in oxidative stress, immunity, and cancer development.Cell communication and signaling : CCS · 2025Review
- Circadian clocks and adaptive immune function: from mechanisms to therapeutic applications.Frontiers in immunology · 2025Review
- Prediction of lung adenocarcinoma prognosis and diagnosis with a novel model anchored in circadian clock-related genes.Scientific reports · 2024Article
- Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.Journal of cellular and molecular medicine · 2024Article
- Sex hormone imbalance and rheumatoid arthritis in American men: a cross-sectional analysis from NHANES 2011-2016.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease with symptoms characterized by typical circadian rhythmic changes. This study aimed to identify the hub circadian rhythm genes (CRGs) in RA and explore their association with immune cell infiltration and pathogenesis of RA. Methods: The differentially expressed CRGs (DECRGs) between RA and normal control samples were screened from Datasets GSE12021 and GSE55235. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis were used to explore the potential functional mechanisms of DECRGs in RA. Weighted Gene Co-expression Network Analysis and Least Absolute Shrinkage and Selection Operator regression analysis were performed to identify hub CRGs of RA. CIBERSORT was conducted to compare the infiltration level of immune cells in RA and control synovial tissue and their relationship with hub genes. In addition, the diagnostic value of hub biomarkers was evaluated by the area under the receiver operator characteristic curve. Further, a nomogram prediction model was constructed and its significance for clinical decision-making was evaluated. Results: The green module was identified as the hub module associated with RA. Four hub CRGs (EGR1, FOSL2, GADD45B, and NFIL3) were identified and showed that they had the highest specificity and sensitivity for RA diagnosis, respectively. The expression levels and diagnostic values of these genes were externally validated in the dataset GSE55457. A nomogram prediction model based on the four hub CRGs was constructed and proved to have a certain clinical decision value. Additionally, the correlation analysis of immune cells with hub genes showed that all hub genes were significantly positively correlated with activated mast cells, resting memory CD4+ T cells, and monocytes. Whereas, all hub genes were negatively correlated with plasma cells, CD8+ T cells, and activated memory CD4+ T cells. Meanwhile, FOSL2 and GADD45B were negatively correlated with Tfh cells. Conclusion: Four hub CRGs were identified and showed excellent diagnostic value for RA. These genes may be involved in the pathological process of RA by disrupting the rhythmic oscillations of cytokines through immune-related pathways and could be considered molecular targets for future chronotherapy against RA.
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