Haoyu Yang, Xunhao Wang, Jiayan Zhu, Yuzhou Liu, Gang Zhao, Jingyi Mi
{"title":"Antimigratory, Anti-Invasive and Anti-Inflammatory Effects of Bergenin in Rheumatoid Arthritis by Downregulating the Wnt/β-Catenin Pathway","authors":"Haoyu Yang, Xunhao Wang, Jiayan Zhu, Yuzhou Liu, Gang Zhao, Jingyi Mi","doi":"10.1111/1756-185x.70360","DOIUrl":"https://doi.org/10.1111/1756-185x.70360","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study investigates antimigratory, anti-invasive, and anti-inflammatory mechanisms of Bergenin in patients with rheumatoid arthritis (RA) by focusing on the pathways involved.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In vitro, TNF-α-induced MH7A cells were used to assess Bergenin's effects on cell proliferation (CCK-8), migration (wound healing, Transwell assays), and apoptosis (flow cytometry). mRNA levels of IL-6 and MMPs were quantified by qRT-PCR, and protein expression was analyzed using ELISA and western blot. The Wnt/β-catenin pathway was examined through immunofluorescence and western blotting with or without LiCl. An adjuvant-induced arthritis (AIA) rat model was used to monitor clinical symptoms and analyze synovial tissue.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Bergenin inhibited the proliferation, migration, and invasion of TNF-α-induced MH7A cells, while promoting apoptosis. It reduced IL-6 and MMPs expression, with these effects reversed by LiCl. In vivo, Bergenin alleviated paw swelling, arthritis score, and synovial pathology in AIA rats, reducing pro-inflammatory factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Bergenin exerts antimigratory, anti-invasive, and anti-inflammatory effects in rheumatoid arthritis by modulating the Wnt/β-catenin pathway, suggesting its potential as a therapeutic option for rheumatoid arthritis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Palmitoylation Dynamics in Systemic Lupus Erythematosus: Multi-Omics Insights and Potential Therapeutic Implications","authors":"Zeyu Liu, Yanggang Hong, Guo Hua, Zixi Li, Chunyan Hua, Sheng Gao","doi":"10.1111/1756-185X.70346","DOIUrl":"https://doi.org/10.1111/1756-185X.70346","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by immune dysregulation. The role of palmitoylation in regulating immune responses and its contribution to SLE pathogenesis remains insufficiently understood.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a multi-omics analysis using the GSE61635 dataset to identify differentially expressed genes (DEGs) in SLE. Palmitoylation-related genes (PRGs) were identified through differential expression analysis, weighted gene co-expression network analysis (WGCNA), and machine learning models. Single-cell RNA sequencing (scRNA-seq) was used to assess immune cell dynamics, and Mendelian randomization (MR) was employed to explore causal relationships between metabolites and SLE.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified 3946 DEGs and 13 key PRGs associated with palmitoylation in SLE. Four hub genes (ACSL1, ZDHHC12, GPX1, and DDHD2) were highlighted as potential biomarkers. Functional enrichment analysis revealed that these genes are involved in fatty acid metabolism and immune signaling. scRNA-seq analysis showed increased palmitoylation activity in neutrophils and cytotoxic T lymphocytes (CTLs) in SLE. MR analysis identified four phospholipids containing palmitic acid as causally linked to SLE.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study identifies ACSL1 and ZDHHC12 as potential therapeutic targets for modulating palmitoylation and immune responses in SLE. Further research is required to validate these findings and explore their clinical implications for SLE treatment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144550851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Junjie Cao, Aifang Li, Gaiying Luo, Zhen Wu, Yuan Liu
{"title":"Decoding PANoptosis in Gout: Signature Gene Identification and Immune Infiltration Profiling","authors":"Junjie Cao, Aifang Li, Gaiying Luo, Zhen Wu, Yuan Liu","doi":"10.1111/1756-185X.70344","DOIUrl":"https://doi.org/10.1111/1756-185X.70344","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Gout is an inflammatory disorder triggered by the deposition of monosodium urate (MSU) crystals in joints and periarticular tissues. PANoptosis, a recently identified form of inflammatory cell death, remains uncharacterized in gout pathogenesis. This study aims to identify PANoptosis-related genes that may drive gout progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Gout-related datasets, including the human cohort (GSE160170) and murine model (GSE190138), were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened using thresholds of |log<sub>2</sub> fold change (FC)| ≥ 1 and adjusted <i>P</i>-value < 0.05. PANoptosis-related biomarkers were identified through the combined use of MCODE and cytoHubba algorithms in Cytoscape. Least Absolute Shrinkage and Selection Operator (LASSO) regression was applied to select hub genes. Subsequently, we performed single—sample gene set enrichment analysis (ssGSEA) for the hub genes, analyzed the infiltration levels of immune cells, constructed a miRNA–mRNA–transcription factor (TF) regulatory network, and identified potential therapeutic drugs via the DSigDB database and the Coremine Medical database. Finally, the expression of the diagnostic gene was validated by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The PANoptosis-associated gene <i>SOCS3</i> was identified via integrative bioinformatics screening. Enrichment analysis and immune infiltration assessment revealed its involvement in gout pathogenesis through pathways linked to inflammation and cell death, with significant correlations observed with specific immune cell subsets. Clinical validation via RT-qPCR confirmed a strong consistency between SOCS3 expression levels in gout patients and computational predictions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We identified the hub gene <i>SOCS3</i> in gout and elucidated its mechanistic roles by integrated bioinformatics analysis, machine learning approach, and clinical validation, providing critical insights for advancing diagnostic biomarkers and therapeutic strategies in gout management.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70344","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144550852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Endophilin A2, a Potential Therapeutic Target for Lupus, Promotes Lupus Progression","authors":"Lu-Qi Yang, You-Yu Lan, You-Qiang Wang, Si-Yu Feng, An-Fang Huang, Wang-Dong Xu","doi":"10.1111/1756-185X.70343","DOIUrl":"https://doi.org/10.1111/1756-185X.70343","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Endophilin A2 (EPA2) is a member of the Endophilin family. The relationship between EPA2 and SLE pathogenesis is unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Plasma levels of EPA2 in SLE patients and healthy controls were detected by ELISA, and EPA2 mRNA levels of SLE patients were explored by qRT-PCR. EPA2 siRNA adenovirus was further injected into pristane-induced lupus mice, and the histological and serological changes were observed. In vitro, EPA2 siRNA adenovirus was transfected to human umbilical vein endothelial cells (HUVECs) in the presence of growth differentiation factor 15 (GDF15), and the proliferation, migration, and tube-forming ability of HUVECs were discussed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Plasma EPA2 levels were significantly higher in SLE patients than in healthy controls (<i>p</i> < 0.001), and EPA2 mRNA levels were significantly higher in SLE patients than in healthy controls as well (<i>p</i> = 0.030). Lupus mice exhibited splenomegaly, severe histologic damage, and high levels of autoantibodies (antinuclear antibody (ANA), anti-double-stranded DNA antibody (anti-dsDNA), and immunoglobulin G (IgG)) (vs. the control group, all <i>p</i> < 0.05). After injection of EPA2 siRNA adenoviruses, the lupus mice showed a lower proportion of CD11b<sup>+</sup>LY-6C<sup>+</sup>, F4/80<sup>+</sup>, CD11c<sup>+</sup>, CD19<sup>+</sup>, CD8<sup>+</sup>, Th1<sup>+</sup>, Th2<sup>+</sup>, Th17<sup>+</sup> cells and reduced expression of pro-inflammatory cytokines, and autoantibodies (vs. the adenoviral empty vector group, all <i>p</i> < 0.05). Addition of EPA2 siRNA adenovirus to HUVECs resulted in decreased GDF15 mRNA levels and reduced cell proliferation, migration and tube formation. However, in the presence of GDF15, EPA2-mediated effects were reversed, and the proliferation, migration, and tube formation ability of HUVECs were enhanced.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>EPA2 may regulate angiogenesis through GDF15, and then involve in SLE pathogenesis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bodhibrata Banerjee, Godasi S. R. S. N. K. Naidu, Rajender Kumar, Aman Sharma
{"title":"Red Hot Ears: An Entity Not to be Missed","authors":"Bodhibrata Banerjee, Godasi S. R. S. N. K. Naidu, Rajender Kumar, Aman Sharma","doi":"10.1111/1756-185X.70264","DOIUrl":"https://doi.org/10.1111/1756-185X.70264","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qi Zheng, Yiping Xu, Xubo Qian, Bin Hu, Qian Ma, Li Guo, Robert M. Dorazio, Meiping Lu
{"title":"Alterations of Gut Microbiome and Serum Short-Chain Fatty Acids in Children With Enthesitis-Related Arthritis","authors":"Qi Zheng, Yiping Xu, Xubo Qian, Bin Hu, Qian Ma, Li Guo, Robert M. Dorazio, Meiping Lu","doi":"10.1111/1756-185X.70337","DOIUrl":"https://doi.org/10.1111/1756-185X.70337","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C. A. Mansoor, Ayman H. K. Alserr, Amal Ibrahim Abdel Latif Mohamed, Hashim Ahmed Ba Wazir
{"title":"Endocarditis Presenting as Arthritis With Positive Autoantibodies Mimicking Rheumatoid Arthritis","authors":"C. A. Mansoor, Ayman H. K. Alserr, Amal Ibrahim Abdel Latif Mohamed, Hashim Ahmed Ba Wazir","doi":"10.1111/1756-185X.70339","DOIUrl":"https://doi.org/10.1111/1756-185X.70339","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Comment on “Comparative Effectiveness of TNF-α and IL-6 Inhibitors on Bone Health Outcomes and Mortality in Rheumatoid Arthritis Patients”","authors":"Saraswati Sah, Rachana Mehta, Ranjana Sah","doi":"10.1111/1756-185X.70355","DOIUrl":"https://doi.org/10.1111/1756-185X.70355","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}