Arthritis Research & Therapy最新文献

{"title":"Real-world data on the use of the Shingrix vaccine among patients with inflammatory arthritis and risk of cardiovascular events following herpes zoster","authors":"Jeffrey R. Curtis, Danielle M. Conrad, Whitney S. Krueger, Andrew P. Gara, Kevin L. Winthrop","doi":"10.1186/s13075-025-03565-0","DOIUrl":"https://doi.org/10.1186/s13075-025-03565-0","url":null,"abstract":"Risk of cardiovascular events may increase after herpes zoster; therefore, American College of Rheumatology guidelines strongly recommend vaccination against herpes zoster in patients aged ≥ 18 years with rheumatic and musculoskeletal diseases taking immunosuppressive medications. Here, we investigated the effectiveness of Shingrix among patients with inflammatory arthritis and estimated the post-herpes zoster risk of cardiovascular events. In this retrospective observational cohort study, data were obtained from the Optum™ Clinformatics™ Data Mart on patients aged ≥ 18 years with rheumatoid arthritis, psoriatic arthritis, or axial spondyloarthritis. The proportions of patients receiving any Shingrix dose, a second dose, and a second dose within 6, 9, and 12 months were calculated. Incidence of herpes zoster following inflammatory arthritis diagnosis was reported. Vaccine effectiveness was calculated as (1 – incidence rate ratio of herpes zoster) × 100. Relative risk of cardiovascular events was assessed independently in the 30-, 45-, 60-, and 90-day periods post-herpes zoster in a subgroup of patients who experienced cardiovascular events. The final cohort included 132,672 patients with inflammatory arthritis. Mean age was 60.4 years, 71.9% were female, and 80.0% were diagnosed with rheumatoid arthritis. Overall, 28,690 (21.6%) patients received ≥ 1 Shingrix dose, of whom only 73.2% received a second dose. Of those receiving a second dose, 17,598 (83.8%) received it within the recommended 2–6 months after the first. Herpes zoster occurred in 4,342 (3.3%) patients, of which 360 cases occurred after Shingrix vaccination. The incidence rate (95% confidence interval) of herpes zoster per 1,000 person-years was 7.41 (6.64, 8.17) after any Shingrix vaccination vs. 14.76 (14.30, 15.22) without vaccination (crude vaccine effectiveness: 50%). The risk of venous thromboembolic events was elevated in the 60–90 days post-herpes zoster; no significantly increased risk was observed for any other cardiovascular events. This study showed that the effectiveness of Shingrix in patients with inflammatory arthritis on immunomodulatory treatment was 50%, and the risk of venous thromboembolic events was increased in the 60–90 days after herpes zoster, supporting the recommendation that adults with inflammatory arthritis should receive vaccination against herpes zoster to reduce the risk of such events.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"96 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond symptomatic alignment: evaluating the integration of causal mechanisms in matching animal models with human pathotypes in osteoarthritis research","authors":"Eva Reihs, Anita Fischer, Iris Gerner, Reinhard Windhager, Stefan Toegel, Frank Zaucke, Mario Rothbauer, Florien Jenner","doi":"10.1186/s13075-025-03561-4","DOIUrl":"https://doi.org/10.1186/s13075-025-03561-4","url":null,"abstract":"Osteoarthritis (OA) is a highly prevalent and disabling condition lacking curative treatments, with only symptomatic relief available. Recognizing OA as a heterogenous disorder with diverse aetiologies and molecular foundations underscores the need to classify patients by both phenotypes and molecular pathomechanisms (endotypes). Such stratification could enable the development of targeted therapies to surmount existing treatment barriers. From a scientific, economic, and ethical perspective, it is crucial to employ animal models that accurately represent the endotype of the target patient population, not merely their clinical symptoms. These models must also account for intrinsic and extrinsic factors, like age, sex, metabolic status, and comorbidities, which impact OA's pathogenesis and its clinical and molecular variability and can profoundly influence not only structural and symptomatic disease severity and progression but also the underlying molecular pathophysiology. The molecular definition of the OA subpopulation must also be reflected in the read-outs, as the traditional methods—macroscopic and histological scoring, along with limited gene expression profiling of established biomarkers for cartilage degradation, extracellular matrix (ECM) turnover, and synovial inflammation—are inadequate for discovering new, phenotype- and endotype-specific biomarkers or therapeutic targets. Thus, animal model characterisation should evolve to include both clinically and pathophysiologically pertinent measures of disease progression and response to treatment. This review evaluates the utility and accuracy of current animal models in OA research, focusing on their capacity to replicate the disease’s pathophysiological processes. ","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"37 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endotheliopathy in systemic sclerosis: from endothelium-dependent vasodilation to the dysfunction of the vascular reserve, is the paradise lost?","authors":"Giulia Bandini, Silvia Bellando Randone, Mirko Manetti, Lorenzo Dagna, Marco Matucci Cerinic, Alberto Moggi Pignone","doi":"10.1186/s13075-025-03568-x","DOIUrl":"https://doi.org/10.1186/s13075-025-03568-x","url":null,"abstract":"Microvascular dysfunction is considered one of the main pathogenetic pathways in systemic sclerosis (SSc), and endothelial cells plays a pivotal role even in the early phases of the disease. Endothelial dysfunction results in an early incapacity to adapt the vascular tone and the blood flow under stress conditions, thus losing the important adaptation mechanism that is the vascular reserve. The loss of vascular tone control in systemic sclerosis is clinically evident as Raynaud’s phenomenon, one of the earliest signs of the disease. An impairment of the vascular reserve has been described in the literature for the main SSc target organs. An alteration of the coronary reserve was shown in SSc asymptomatic patients undergoing a provocative cardiac stress tests. For what concerns the pulmonary circulation, in presence of normal resting pulmonary pressure values in specific subsets of SSc patients subjected to a cycle ergometer test, an abnormal elevation of pulmonary pressure has been showed. Regarding renal arterial circulation, in SSc patients with normal baseline renal function, an absence of improved glomerular filtration after the infusion of a protein load has been demonstrated. Finally, vascular reserve can be altered even in the gastrointestinal circulation as assessed by the study of the splanchnic circulation after a balanced meal. An early detection of an alteration of the physiologic protective mechanism of the vascular reserve could open a “window of opportunity” in which SSc vasculopathy can be potentially reversible, and more responsive to targeted therapeutic strategies.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"30 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vagotomy and the incidence of rheumatoid arthritis and osteoarthritis: a Danish register-based study","authors":"Matthew C. Baker, Dávid Nagy, Suzanne Tamang, Erzsébet Horváth-Puhó, Henrik Toft Sørensen","doi":"10.1186/s13075-025-03567-y","DOIUrl":"https://doi.org/10.1186/s13075-025-03567-y","url":null,"abstract":"Given the potential role of vagus nerve stimulation in treating rheumatoid arthritis (RA), we examined the incidence of RA and osteoarthritis (OA) in patients who underwent different forms of vagotomy that disparately affect the inflammatory reflex. Using nationwide health registries, we constructed cohorts of patients in Denmark who underwent truncal or superselective vagotomy between 1977 and 1995 and comparison members from the general population matched 10:1 on birth year, sex, and calendar year. We identified incident RA or OA and used Cox proportional hazards models to compute adjusted hazard ratios (aHRs) and corresponding 95% CI. Our cohorts consisted of 2,260 truncal vagotomy patients matched with 22,610 comparators, and 3,810 superselective vagotomy patients matched with 38,090 comparators. The incidence rate (IR) of RA per 1,000 person-years (95% CI) in the truncal vagotomy cohort was 10.2 (6.5–15.3) versus 7.2 (6.1–8.4) in the matched comparison cohort. The aHR (95% CI) for RA development was 2.62 (1.47–4.67) in the truncal vagotomy cohort and 1.05 (0.51–2.17) in the superselective vagotomy cohort, with respect to comparison cohorts. The risk of developing OA was not significantly different for either vagotomy cohort compared with comparison cohorts. Truncal vagotomy was associated with an increased incidence of RA; this association was not observed with superselective vagotomy. No association with either form of vagotomy was seen with OA. These findings support the hypothesis that disruption of vagus nerve signaling impacts the inflammatory reflex and contributes to the development of RA.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"5 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atf3 + senescent chondrocytes mediate meniscus degeneration in aging","authors":"Jing-Yi Wang, Yao-Hui Liu, Xiao Wang, Min Ma, Zhang-Yi Pan, Ao-Yuan Fan, Lai-Ya Lu, Zheng Liu, Kun Tao, Feng Yin","doi":"10.1186/s13075-025-03566-z","DOIUrl":"https://doi.org/10.1186/s13075-025-03566-z","url":null,"abstract":"Meniscus degeneration contributes to knee arthritis progression, but the cellular and molecular mechanisms of meniscus aging remain poorly understood. We aimed to characterize age-related changes in the rat meniscus using single-cell RNA sequencing (scRNA-seq) and identify key pathogenic cell populations and pathways. Meniscal tissues from young (12 weeks) and aged (24 months) rats were processed for histology, flow cytometry, and scRNA-seq. Bioinformatics tools, including Seurat, Monocle 2, and CellChat, were used to analyze cellular composition, pseudotime trajectories, and intercellular communication. Senescence-related features and signaling pathways were evaluated. Knee joint of aged rats exhibited higher Osteoarthritis Research Society International (OARSI) scores and synovial inflammation. scRNA-seq revealed three major chondrocyte subpopulations: Sox9 + stable chondrocytes, Fndc1 + fibrochondrocytes, and Atf3 + senescent chondrocytes. Aging caused a significant increase in Atf3 + senescent chondrocytes, characterized by the expression of senescence markers (Cdkn1a/Cdkn2a) and activation of inflammatory pathways such as tumor necrosis factor (TNF) and nuclear factor-κB (NF-κB). These cells were predominantly located at the endpoint of differentiation trajectories. CellChat analysis identified the ANGPTL4-SDC4 axis as a key signaling pathway mediated by Atf3 + cells. Immunostaining confirmed elevated Angiopoietin-Like Protein 4 (ANGPTL4) expression in aged menisci. We identified Atf3 + senescent chondrocytes as a key pathogenic population in the aging meniscus, driving degeneration via the ANGPTL4 pathway. Targeting Atf3 + cells or ANGPTL4 signaling may offer new therapeutic strategies for age-related meniscus degeneration and arthritis.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"114 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143979776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chondrocyte lysates activate NLRP3 inflammasome-induced pyroptosis in synovial fibroblasts to exacerbate knee synovitis by downregulating caveolin-1","authors":"Xue Du, Ruonan Liu, Zongrui Jiang, Chengyun Zhang, Zhijian Yang, Shu Hu, Zhiqi Zhang","doi":"10.1186/s13075-025-03573-0","DOIUrl":"https://doi.org/10.1186/s13075-025-03573-0","url":null,"abstract":"Synovitis, among the most common signs of early-stage osteoarthritis (OA), is mainly mediated by fibroblast-like synoviocytes (FLSs). Cartilage destruction creates chondrocyte lysates (CLs) that activate synovial inflammation. A comprehensive understanding of chondrocyte–FLS communication might offer novel, specific therapeutic targets for treating synovitis and OA. Hence, we sought to uncover the specific role of CLs in OA-FLSs and synovitis. Isolated CLs were cocultured with FLSs to test whether they could stimulate synovial inflammation. A model of medial meniscus destabilization was prepared in C57BL/6 mice and NLRP3 knockout mice, and adeno-associated virus overexpressing Caveolin-1 (CAV1) was intra-articularly injected for 8 weeks once a week after dissection of the medial meniscus (DMM). Proteins expressed in FLSs with and without CL coculture were screened using liquid chromatography-tandem mass spectrometry to identify CL-specific regulators of NLRP3 inflammasome-mediated pyroptosis. CLs were engulfed by FLSs, which aggravated inflammatory cytokine release and NLRP3 inflammasome-mediated FLS pyroptosis. NLRP3 expression was significantly upregulated in human OA-FLSs and FLSs cocultured with CLs, while CAV1 was downregulated. CAV1 overexpression reversed the inflammatory phenotype in FLSs and simultaneously rescued pyroptosis in CL-pre-treated FLSs. Both synovial hyperplasia and inflammatory infiltration in C57BL/6 mice with DMM surgery were alleviated after intra-articular AAV-CAV1 injection. Moreover, the CL-specific protein LIM-containing lipoma preferred partner (LPP) markedly exacerbated FLS pyroptosis and inflammation. CLs were endocytosed by FLSs through CAV1, and the CL-specific protein LPP stimulated NLRP3 inflammasome-mediated pyroptosis and synovitis by inhibiting CAV1 expression. Our findings offer a novel therapeutic target for treating synovitis.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"14 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143979780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gender differences in clinical and prescribing characteristics of biologic and targeted synthetic drugs in naïve patients with rheumatoid arthritis: Data from BIOBADASER III registry","authors":"Paloma Vela-Casasempere, Lucía Otero-Varela, Silvia Gómez Sabater, Rocío Caño Alameda, Cristina Campos Fernández, Jerusalén Calvo-Gutiérrez, Yanira Pérez-Vera, Sara Manrique Arija, Sagrario Bustabad, Javier Manero Ruiz, María Dolores Ruiz Montesino, Lucía Ruíz Gutiérrez, Antonio Mera Varela, Manuel José Moreno Ramos, Fernando Sánchez-Alonso, Isabel Castrejón","doi":"10.1186/s13075-025-03571-2","DOIUrl":"https://doi.org/10.1186/s13075-025-03571-2","url":null,"abstract":"Rheumatoid arthritis (RA) is a chronic systemic inflammatory autoimmune disease that can lead to progressive joint damage and irreversible disability when inadequately treated. RA is more common in women than in men. Disease characteristics differ between genders in terms of comorbidities, extra-articular manifestations, quality of life, disease activity and functional scores. There is a possibility that RA may be managed differently depending on gender: under-treated due to professional bias when prescribing advanced therapies, or over-treated due to overestimation of disease activity. Our primary objective was therefore to examine gender differences in the time course from RA diagnosis to initiation of the first biologic disease-modifying antirheumatic drug (bDMARD) or targeted synthetic DMARD (tsDMARD) and to identify factors associated with earlier or later prescribing. We also aimed to assess the differences between men and women in clinical characteristics and disease activity at initiation of the first b/tsDMARD among bio-naïve RA patients. We analyzed RA patients from the BIOBADASER III registry who began their first b/tsDMARD between 2000 and 2023, stratified by treatment start year. Clinical characteristics were compared by sex, using linear regression models for DAS28. Kaplan–Meier curves and multivariate Cox regression identified factors influencing treatment initiation timelines. We included 3,384 patients (78.1% women). Males presented higher cardiovascular risk, females more osteoporosis and Sjögren Syndrome. At treatment start, females had lower mean age (54.8 vs. 57 years, p < 0.001) but longer disease duration (7.3 vs. 6.7 years, p = 0.031); higher DAS28-ESR, but not DAS28-CRP; higher subjective components of DAS28 and ESR but lower CRP and no differences in objective components. Disease duration differed between sexes only in the most recent cohort (≥ 2017, HR 0.9 (95% CI 0.81; 0.99), p = 0.026): female sex, age, and treatment with csDMARDs (other than methotrexate) were associated with later prescribing, whereas tobacco, obesity and treatment with methotrexate or glucocorticoids with earlier. Later prescribing in women despite higher activity rates merits reflection. Discrepancies between subjective and objective measures of DAS, and ESR and CRP, may reflect the need to establish different cut-off points for men and women, and opens a field of research worth exploring.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"52 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143945903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAR-T cell therapy for juvenile-onset autoimmune diseases: a promising future?","authors":"Maurine Jouret, Sebastien Viel, Benjamin Fournier, Sarah Benezech, Jérome Avouac, Marc Scherlinger, Alexandre Belot","doi":"10.1186/s13075-025-03564-1","DOIUrl":"https://doi.org/10.1186/s13075-025-03564-1","url":null,"abstract":"Chimeric antigen receptor (CAR) T-cell therapy targeting B cells has shown promising results, including drug-free remission, in adult-onset autoimmune diseases. Extending this therapeutic approach to the pediatric population, particularly for juvenile autoimmune diseases, presents an exciting opportunity. However, challenges specific to juvenile-onset autoimmune conditions, such as long-term adverse events, heightened disease activity, and the imperative to reduce steroid exposure, must be considered. While this strategy appears viable for these severe conditions, the limited data available for this population and the absence of evidence on cases with a high genetic component, such as monogenic lupus, represent significant challenges. Most monogenic lupus cases are associated with innate immune defects, and the involvement of B cells in these genetic anomalies remains poorly understood. In this review, we examine the potential indications, current knowledge, and limitations of CAR-T cell therapy in juvenile-onset autoimmune diseases, extending the discussion beyond early-onset lupus.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"1 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Smoking as a risk factor for rheumatoid arthritis: predominant association with IgA autoantibodies – comprehensive analysis of anti-modified protein antibodies with smoking and genetic risk factors in rheumatoid arthritis","authors":"Tineke J. van Wesemael, Fraser R. Morton, Judith W. Heutz, Marc P. Maurits, Annemarie L. Dorjée, Duncan Porter, Tom W. J. Huizinga, Karim Raza, Rene E. M. Toes, Rachel Knevel, Pascal H. P. de Jong, Anna Svärd, Diane van der Woude","doi":"10.1186/s13075-025-03543-6","DOIUrl":"https://doi.org/10.1186/s13075-025-03543-6","url":null,"abstract":"Rheumatoid arthritis (RA) is an autoimmune disease characterized by the presence of autoantibodies against modified proteins, known as anti-modified protein autoantibodies (AMPAs). While the relationship between different AMPA isotypes and various risk factors remains poorly understood, investigating this association is important for a deeper understanding of RA pathophysiology. Smoking, has its primary effects in the lungs, and it remains unclear whether smoking is preferentially linked to specific AMPA isotypes, such as IgA, which could suggest a mucosal origin. Therefore, we set out to investigate the association between smoking, genetic risk factors for RA, and the presence of specific AMPA isotypes, particular IgA. In 618 RA patients, anti-citrullinated protein antibodies (ACPA-) and anti-acetylated protein antibodies (AAPA-) IgA, -IgG and -IgM and RF-IgA and -IgM were measured by ELISA. Associations with genetic risk factors, smoking and autoantibodies were assessed with logistic regression analysis. For replication, a comprehensive meta-analysis incorporating 3309 RA patients was performed. Smoking was primarily associated with IgA AMPA, with associations that prevailed after correcting for the concurrent presence of AMPA IgG (ACPA-IgA OR 1.89 [1.14–3.12], AAPA-IgA 2.30 [1.35–3.94]). To further substantiate these results, we performed a meta-analysis of 3309 RA patients and observed that smoking was again predominantly associated with the combined presence of ACPA-IgA in addition to ACPA-IgG (OR 2.05 [1.69–2.49], p < 0.001) versus the single presence of ACPA-IgG (OR 1.18 [0.97–1.44], p = 0.11). A gene-environment interaction between the most important genetic risk factor for RA (the HLA shared epitope alleles) and smoking was only seen in patients that were both ACPA-IgG and ACPA-IgA positive, but not in patients who were only positive for ACPA-IgG. These data provide a pivotal refinement of existing knowledge regarding risk factor associations for RA and lend novel support to the hypothesis that smoking may exert its effect on RA by the induction of local (auto)immune responses at mucosal sites.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"48 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in omics and the integration of multi-omics in osteoarthritis research","authors":"Ye Liu, Vladimir Molchanov, David Brass, Tao Yang","doi":"10.1186/s13075-025-03563-2","DOIUrl":"https://doi.org/10.1186/s13075-025-03563-2","url":null,"abstract":"Osteoarthritis (OA) is a complex disorder driven by the combination of environmental and genetic factors. Given its high global prevalence and heterogeneity, developing effective and personalized treatment methods is crucial. This requires identifying new disease mechanisms, drug targets, and biomarkers. Various omics approaches have been applied to identify OA-related genes, pathways, and biomarkers, including genomics, epigenomics, transcriptomics, proteomics, and metabolomics. These omics studies have generated vast datasets that are shaping the field of OA research. The emergence of high-resolution methodologies, such as single-cell and spatial omics techniques, further enhances our ability to dissect molecular complexities within the OA microenvironment. By integrating these multi-layered datasets, researchers can uncover central signaling hubs and disease mechanisms, ultimately facilitating the development of targeted therapies and precision medicine approaches for OA treatment.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"48 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143901789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}