Arthritis Research & Therapy最新文献

{"title":"Cluster analysis reveals three clinical phenotypes of pulmonary artery hypertension associated with connective tissue diseases: insights into inflammation and immunity","authors":"Qianwen Wu, Dongyu Li, Huangshu Ye, Zhangdi Zhou, Yixin Zhang, Miaojia Zhang, Xiaoxuan Sun, Qiang Wang","doi":"10.1186/s13075-025-03545-4","DOIUrl":"https://doi.org/10.1186/s13075-025-03545-4","url":null,"abstract":"Inflammation and immune mechanisms play a crucial role in connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH), though they remain inadequately understood. This study aimed to identify specific clinical phenotypes in CTD-PAH using inflammatory and immune markers through hierarchical cluster analysis. We conducted a single-center, retrospective cohort study of CTD-PAH patients from 2009 to 2024. Clinical variables, including neutrophil lymphocyte ratio (NLR), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and complement C3 and C4, were analyzed to form clusters based on baseline characteristics, clinical outcomes, and treatment goals. Among 184 patients (95.1% female; median age 40.42 years), three distinct clusters were identified: Cluster 1 (vasculopathic phenotype) exhibited lower inflammatory activity but worse hemodynamic outcomes; Cluster 2 (vasculitic phenotype) had higher inflammatory activity with favorable hemodynamics; Cluster 3 (mixed phenotype) showed active inflammation and poor hemodynamic status. Most vasculitic patients were classified as systemic lupus erythematosus-associated PAH (SLE-PAH), which had a shorter course and higher prevalence of autoantibodies. The vasculopathic and mixed phenotypes were common in scleroderma-related PAH (SSc-PAH), undifferentiated CTD- related PAH (UCTD-PAH), and mixed CTD- related PAH (MCTD-PAH), associated with poorer treatment outcomes and survival rate. Distinct clinical phenotypes in CTD-PAH correlate with inflammatory activity and hemodynamic status, influencing treatment responses and prognosis. Inflammation and immune mechanisms are essential for the development of CTD-PAH. Three distinct phenotypes in CTD-PAH were identified through cluster analysis. Distinct phenotypes correlate with inflammatory and hemodynamic status, influencing treatment responses and prognosis. Identifying disease phenotypes might improve the management algorithm for CTD-PAH.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"108 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782587","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":"Infrapatellar fat pad as a source of biomarkers and therapeutic target for knee osteoarthritis","authors":"Betzabeth Pereira Herrera, Kaj Emanuel, Pieter J. Emans, Martijn van Griensven, Berta Cillero-Pastor","doi":"10.1186/s13075-025-03517-8","DOIUrl":"https://doi.org/10.1186/s13075-025-03517-8","url":null,"abstract":"Osteoarthritis (OA) is a multifactorial and highly prevalent disease in elderly adults; however, its pathogenesis, diagnosis, and treatment are unmet needs nowadays. Research efforts have focused on elucidating the molecular mechanisms involved in the pathogenesis, onset, and progression of OA to facilitate early detection and effective therapeutic approaches. Infrapatellar fat pad (IPFP) represents a promising novel source of OA biomarkers given that it is an active player in OA. This review aims to investigate the current literature regarding the potential of the IPFP as a source of diagnostic and prognostic biomarkers for OA as well as potential target for novel therapies. A literature search was conducted in the PubMed database in June 2024. We included cross-sectional and longitudinal studies based on IPFP from human OA patients, oriented in the identification of imaging, biochemical, and molecular biomarkers in the IPFP. After screening and evaluation, we included a total of 61 studies. Most of the imaging publications (n = 47) on IPFP are based on magnetic resonance imaging (MRI) that revealed potential semiquantitative and quantitative imaging biomarkers linked to inflammation, fibrosis, pain, and joint degeneration imaging parameters. Biochemical and molecular studies (n = 14) pointed out an increase in interleukin-6 (IL-6), fatty acid-binding protein 4 (FABP4), adiponectin, and lysophosphatidylcholine (LysoPC) in the IPFP during OA progression. Imaging, biochemical, and molecular studies indicate OA potential biomarkers in the IPFP related to inflammation, lipid dysregulation, and fibrosis. The combination of imaging and biochemical biomarkers could provide a better prediction of OA onset and the identification of OA progressors at an early stage. The IPFP study could also reveal potential therapeutic targets with the vision of better precision medicine.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"34 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782573","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":"Concomitant Sjögren’s disease in patients with NMOSD: impacts on neurologic disease severity and recurrence","authors":"Wanqing Wu, Wenbo Yang, Bo Deng, Helian Li, Xiaoni Liu, Hai Yu, Xiang Zhang, Minrui Liang, Xiangjun Chen","doi":"10.1186/s13075-025-03538-3","DOIUrl":"https://doi.org/10.1186/s13075-025-03538-3","url":null,"abstract":"We aimed to characterize the phenotype of neuromyelitis optica spectrum disorder (NMOSD) in the presence and absence of Sjogren's disease (SjD) and to develop a predictive nomogram to evaluate the risk of coexisting SjD within a single tertiary-center cohort of NMOSD patients. Paraclinical and clinical features of patients with SjD were compared between NMOSD patients with SjD and those without SjD. Zstats v1.0 was utilized to randomly allocate participants into a derivation group (108 patients) and a validation group (47 patients) at a ratio of 7:3. Logistic regression analysis was used to assess the effectiveness of our predictive model, and a nomogram was created to illustrate the findings. A total of 155 NMOSD patients who were serologically positive for AQP4-IgG were cross-sectionally recruited (70 NMOSD patients with SjD [45.16%] and 85 NMOSD patients without SjD [54.84%]). Independent predictors of coexisting SjD were age upon recruitment (P = 0.002); Expanded Disability Status Scale (EDSS) score (P = 0.023); blood white blood cell (WBC) count (P = 0.049); and rheumatoid factor (RF) (P = 0.049), anti-SSA (Ro), and anti-SSB (La) antibody positivity (P < 0.001; P = 0.012). The nomogram had an area under the receiver operating characteristic (ROC) curve (AUC) (95% confidence interval [CI]) of 0.95 (0.89, 1.00) in the derivation cohort and 0.91 (0.79, 1.00) in the validation cohort. Survival curve analysis revealed that the EDSS score in the NMOSD patients with SjD was associated with clinical relapse, and these patients reached an EDSS score of 4.0 earlier than those without SjD. NMOSD patients with SjD manifested more severe disease at attack and relapsed earlier than those without SjD. The nomogram established by combining age upon recruitment; EDSS score; blood WBC count; and RF, anti-SSA (Ro), and anti-SSB (La) antibody levels can significantly predict the risk of NMOSD combined with SjD.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782580","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":"25 years of research and therapy in arthritis","authors":"Harris Perlman, Christopher D. Buckley","doi":"10.1186/s13075-024-03439-x","DOIUrl":"https://doi.org/10.1186/s13075-024-03439-x","url":null,"abstract":"&lt;p&gt;When it was established 25 years ago by Peter Lipsky and Ravinder Maini, Rheumatology as a speciality, like Cinderella, had just arrived at the ball. Anti TNF therapy was revolutionizing the treatment of not just inflammatory arthritis, but many other immune mediated inflammatory diseases. For the first time people with arthritis could dream of a cure. But to cure a disease requires an understanding of its cause. So two years after we took over as editors in Chief of &lt;i&gt;Arthritis Research and Therapy&lt;/i&gt; we outlined how we wanted the new aims and scope of the Journal to be https://arthritis-research.biomedcentral.com/articles/https://doi.org/10.1186/s13075-018-1518-y to reflect this desire to aim for a cure. We focussed on two themes we wanted to promote: discovery research and experimental therapy. Since 2018 there has been a revolution in the basic, translational and clinical research that has been considered for publication by the journal, driven by advances in spatial technology and single cell analysis as well as artificial intelligence and bioinformatics. All these approaches have helped expose the mechanisms that drive pathogenicity. The ability to sample human tissue using minimally invasive techniques and to do so over time has allowed our authors to submit manuscripts that explore causal mechanisms in the real model organism; humans, in real clinical studies, rather than having to extrapolate from preclinical models in mice. This combined with the explosion in cell-based depletion strategies using CAR T cell therapies, means that our Journal is well placed to continue to lead the way in publishing outstanding research and new studies that explore novel therapies in arthritis into the next 25 years. To do this will require the continued engagement of our international community of outstanding and expert section editors, associate editors and editorial board as well as the selfless commitment of our reviewers. The new editorial management system (SNAPP: Springer Nature’s article Processing platform) has improved our governance and editorial consistency and enhanced the turnaround rate for manuscripts. It also allows us to monitor plagiarism and malpractice during the submission and review process using state of the art AI systems across the full range of Springer Nature Journals. We want to thank all those colleagues who have helped and continue to help the journal become a trusted, internationally respected journal that expands the boundaries of musculoskeletal disease research.&lt;/p&gt;&lt;h3&gt;Authors and Affiliations&lt;/h3&gt;&lt;ol&gt;&lt;li&gt;&lt;p&gt;Department of Medicine, Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA&lt;/p&gt;&lt;p&gt;Harris Perlman&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Kennedy Institute of Rheumatology, , University of Oxford, Roosevelt Drive, Headington, Oxford, UK&lt;/p&gt;&lt;p&gt;Christopher D. Buckley&lt;/p&gt;&lt;/li&gt;&lt;/ol&gt;&lt;span&gt;Authors&lt;/span&gt;&lt;ol&gt;&lt;li&gt;&lt;span&gt;Harris Perlman&lt;/span&gt;View author publications&lt;p&gt;&lt;span&gt;You can also search for this au","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"32 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143757993","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":"Higher levels of VEGF-A and TNFα in patients with immune checkpoint inhibitor-induced inflammatory arthritis","authors":"Elise F. Gray-Gaillard, Ami A. Shah, Clifton O. Bingham III, Jennifer H. Elisseeff, Joseph Murray, Julie Brahmer, Patrick Forde, Valsamo Anagnostou, Jennifer Mammen, Laura C. Cappelli","doi":"10.1186/s13075-025-03546-3","DOIUrl":"https://doi.org/10.1186/s13075-025-03546-3","url":null,"abstract":"Immune checkpoint inhibitors (ICI), a type of cancer immunotherapy, can cause side effects including inflammatory arthritis (ICI-IA). Previous studies of ICI-IA do not include a thorough characterization of associated immune responses to provide potential targets for treatment. We aimed to identify cytokines uniquely increased in ICI-IA and determine correlations with IA severity and persistence. We evaluated patients diagnosed with ICI-IA by a rheumatologist (n = 80); control serum was obtained from ICI-treated cancer patients without any diagnosed irAEs (n = 17) or diagnosed with an unrelated irAE (n = 19). Serum was assayed to quantify 9 cytokine levels (IFN-γ, IL-4, IL-6, IL-10, IL-12p70, IL-1α, TNF-α, IL-17a, VEGF-A) using MSD U-PLEX assay. Mann-Whitney U tests were performed to evaluate differences in cytokine levels between control and ICI-IA groups. The Kruskal-Wallis test and multivariable ordinal logistic regression were used to determine difference in cytokine levels between patients of differing disease activity. VEGF-A and TNFα were significantly elevated in patients with ICI-IA compared to ICI-controls; results persisted when restricting analyses to patients not treated with immunosuppressants at the time of sampling. ICI-IA patients were stratified by IA severity using CDAI score; there was significantly higher VEGF-A in those with higher disease activity. Ordinal logistic regression showed higher levels of IL-6 and VEGF-A were associated with higher disease activity. Elevated levels of VEGF-A and TNFα are associated with ICI-IA. There was also higher IL-6 and VEGF-A among those with higher disease activity when controlling for confounding. These cytokines could be used as biomarkers of ICI-IA severity and present therapeutic targets.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"15 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744827","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":"Modulating IL-21-driven B cell responses in idiopathic inflammatory myopathies via inhibition of the JAK/STAT pathway","authors":"Ana Merino-Vico, Merve Kocyigit, Giulia Frazzei, Lisa Landman, Louis Boon, Ester M. van Leeuwen, Ingrid E. Lundberg, Anneke J. van der Kooi, Joost Raaphorst, Jan Piet van Hamburg, Sander W. Tas","doi":"10.1186/s13075-025-03547-2","DOIUrl":"https://doi.org/10.1186/s13075-025-03547-2","url":null,"abstract":"Idiopathic inflammatory myopathies (IIM) are autoimmune disorders characterized by muscle inflammation and autoreactive B cell responses. The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway is essential for B cell functions, making it a promising therapeutic target. This study explores the potential of tofacitinib, a JAK1/JAK3 inhibitor, to modulate B cell activity in IIM. Peripheral B cell populations from dermatomyositis (DM), anti-synthetase syndrome (ASyS) and overlap myositis (OM) patients were analyzed by flow cytometry. Peripheral blood mononuclear cells (PBMC) or sorted memory B cells were cultured with tofacitinib and stimulated with combinations of CD40, IL-21, IL-2, BAFF and CpG. B cell proliferation, differentiation and (auto)antibody, cytokine/chemokine production were assessed by flow cytometry, Luminex, and ELISA/ELiA assays. The IIM peripheral B cell compartment had elevated transitional and naive B cells, with reduced Bmem frequencies compared to healthy donors. Tofacitinib significantly inhibited CD40/IL-21-induced B cell proliferation, plasmablast formation and function in PBMC and B cell-only cultures across all IIM subgroups, predominantly affecting the IL-21-induced differentiation and antibody production. Remarkably, tofacitinib reduced the levels of anti-Jo1 autoantibodies, as well as of CXCL10 and CXCL13 in ASyS memory B cell cultures. These findings highlight the B cell involvement in IIM, evidenced by altered peripheral B cell composition in active disease and the effective inhibition of essential B cell responses, including proliferation, differentiation, and (auto)antibody production, by tofacitinib in vitro. This positions the JAK/STAT pathway as a promising new therapeutic target to modulate B cell activity in IIM.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143757994","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":"A diagnostic model for assessing the risk of osteoporosis in patients with rheumatoid arthritis based on bone turnover markers","authors":"Yubo Shao, Yazhu Yang, XiaoYu Yang, Zihang Xu, Hong Zhang, Ning Li, Hao Xu, Yongjian Zhao, Yongjun Wang, Qi Shi, Qianqian Liang","doi":"10.1186/s13075-025-03544-5","DOIUrl":"https://doi.org/10.1186/s13075-025-03544-5","url":null,"abstract":"The risk of developing osteoporosis (OP) is increased in patients with rheumatoid arthritis (RA), which is associated with poorer prognosis and higher mortality. Many patients with RA may experience bone loss early in the disease course. Therefore, timely assessment of the risk of OP in RA patients is essential. This is a retrospective study in which we collected information from 500 RA patients who underwent bone mineral density assessments at Longhua Hospital, Shanghai University of Traditional Chinese Medicine, from January 2018 to December 2022. Based on the data collection timeline, the first 70% of patients were assigned to the training set, while the remaining 30% were included in the validation set. The model was established using the training set and evaluated through plotting of the receiver operating characteristic curves, calibration curves, and clinical decision curves. Internal validation was performed by resampling the training set data 1,000 times using the bootstrap method, while internal hold-out validation was conducted using the validation dataset. Ultimately, six variables were identified as independently associated with RA combined with OP (RA-OP): female sex, age, beta C-terminal cross-linked peptide (β-CTX), anti-cyclic citrullinated peptide antibody (ACPA), triglycerides (TG), and N-terminal propeptide of type I procollagen (PINP). The regression equation for the model is as follows: Logistic (RA-OP) = -8.703 + 0.946*female + 0.053*age + 0.004*β-CTX + 0.001*ACPA + 0.6*TG-0.008*PINP. The model demonstrated good discrimination (AUC = 0.819, 95% CI: 0.775–0.863) and calibration. In both internal and internal hold-out validation, the model also performed well, with AUC values of 0.814 (95% CI: 0.772–0.864) and 0.772 (95% CI: 0.697–0.847), respectively. Clinical decision curves indicated that the model outperformed both extreme curves, suggesting good clinical utility. Our model is user-friendly and has shown good predictive performance in both internal and internal hold-out validation, offering new insights for the early screening and treatment of OP risk in RA patients.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"8 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744832","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":"The TLR-M-CSF axis is implicated in increased bone turnover and curve progression in adolescent idiopathic scoliosis","authors":"Kai Sheng, Daniel G. Bisson, Neil Saran, Jake Bourdages, Christopher Coluni, Kirby Upshaw, Kerstin Tiedemann, Svetlana V. Komarova, Jean A. Ouellet, Lisbet Haglund","doi":"10.1186/s13075-025-03535-6","DOIUrl":"https://doi.org/10.1186/s13075-025-03535-6","url":null,"abstract":"Facet joint osteoarthritis (OA) is prevalent in patients with adolescent idiopathic scoliosis (AIS). The most pronounced OA presents above and below the curve's apex where the intervertebral rotation is the greatest. This indicates that facet joint OA is implicated and potentially contributes to AIS progression. OA impacts both cartilage and bone and we have previously demonstrated an association between lower bone quality and more severe OA in AIS facet joints. This study aimed to further investigate the molecular mechanisms underlying cartilage–bone crosstalk in the facet joints of patients with AIS. Unbiased deep RNA sequencing was performed to compare gene expression in facet joint chondrocytes of age-matched AIS patients and non-scoliotic individuals. Differentially expressed genes of interest were validated through qPCR and ELISA in a larger sample cohort. Key regulatory pathways involved in cartilage–bone crosstalk were identified through bioinformatic analysis. Functional studies were conducted by treating chondrocytes with TLR2 and TLR4 agonists, collecting conditioned media, and administering it to an in vitro osteoclastogenesis model. The expression of M-CSF, a key regulatory factor influencing osteoclast proliferation, was measured in individual facet joint cartilage samples at different spinal levels and correlated with cartilage morphological grade and 3D structural parameters extracted from spine reconstruction. One thousand four hundred twenty six upregulated genes were detected, and gene ontology analysis revealed a significant enrichment of the TLR pathway, and bone-regulating biological processes in AIS chondrocytes. TLR activation of AIS chondrocytes induced expression of bone-regulating factors, including M-CSF, a key regulator of osteoclast proliferation. Furthermore, secreted factors from AIS chondrocytes enhanced osteoclast proliferation and maturation, with a stronger effect observed following TLR pre-activation. Clinically, M-CSF expression was found to correlate strongly with increased OA severity and a greater degree of intervertebral axial rotation. Together, our findings suggest that the TLR-M-CSF axis is implicated in osteoclastogenesis, resulting in increased bone turnover and may contribute to curve progression in AIS patients.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"72 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736795","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":"The insula represents a key neurobiological pain hub in psoriatic arthritis","authors":"Flavia Sunzini, Kristian Stefanov, Salim Al-Wasity, Chelsea Kaplan, Andrew Schrepf, Noah Waller, Steven Harte, Richard Harris, Daniel J. Clauw, John McLean, Stefan Siebert, Carl S. Goodyear, Gordon D. Waiter, Neil Basu","doi":"10.1186/s13075-025-03526-7","DOIUrl":"https://doi.org/10.1186/s13075-025-03526-7","url":null,"abstract":"Pain remains a principal complaint for people with psoriatic arthritis (PsA), despite successful mitigation of inflammation. This situation alludes to the co-existence of distinct pain mechanisms. Nociceptive and nociplastic mechanisms are clinically challenging to distinguish. Advances in brain functional magnetic resonance imaging (fMRI) have successfully characterised distinct pain mechanisms across several disorders, in particular implicating the insula. This is the first study to characterise neurobiological markers of pain mechanisms in PsA employing fMRI. PsA participants underwent a 6-minutes resting-state fMRI brain scan, and questionnaire assessments of nociplastic pain (2011 ACR fibromyalgia criteria) and body pain, assessed using the Numeric Rating Scale (NRS, 0-100). Functional connectivity between insula seeds (anterior, mid, posterior), and the whole brain was correlated with the above pain outcomes correcting for age and sex, and false discovery rate (FDR) for multiple comparisons. A total of 46 participants were included (age 49 ± 11.2; 52% female; FM score 12.5 ± 5.7; overall pain 34.8 ± 23.5). PsA participants with higher fibromyalgia scores displayed increased connectivity between: (1) right anterior insula to DMN (P < 0.05), (2) right mid and left posterior insula to parahippocampal gyri (P < 0.01 FDR); and (3) right mid insula to left frontal pole (P = 0.001 FDR). Overall pain was correlated with connectivity of left posterior insula to classical nociceptive regions, including thalamus (P = 0.01 FDR) and brainstem (P = 0.002 FDR). For the first time, we demonstrate objectively that nociceptive and nociplastic pain mechanisms co-exist in PsA. PsA pain cannot be assumed to be only nociceptive in origin and screening for nociplastic pain in the future will inform supplementary analgesic approaches.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"96 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736793","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":"Editorial Expression of Concern: A model of anti-angiogenesis: differential transcriptosome profiling of microvascular endothelial cells from diffuse systemic sclerosis patients","authors":"Betti Giusti, Gabriella Fibbi, Francesca Margheri, Simona Serratì, Luciana Rossi, Filippo Poggi, Ilaria Lapini, Alberto Magi, Angela Del Rosso, Marina Cinelli, Serena Guiducci, Bashar Kahaleh, Laura Bazzichi, Stefano Bombardieri, Marco Matucci-Cerinic, Gian Franco Gensini, Mario Del Rosso, Rosanna Abbate","doi":"10.1186/s13075-025-03549-0","DOIUrl":"https://doi.org/10.1186/s13075-025-03549-0","url":null,"abstract":"&lt;p&gt;&lt;b&gt;Editorial Expression of Concern: Arthritis Res Ther 8&lt;/b&gt;,&lt;b&gt; R115 (2006)&lt;/b&gt;&lt;/p&gt;&lt;p&gt;https://doi.org/10.1186/ar2002&lt;/p&gt;&lt;p&gt;The Editors-in-Chief are issuing an editorial expression of concern to alert readers that panel C in Fig. 3 appears to be very similar to panel H in Fig. 2 in a previously-published article by the same author group [1], but the images are labelled differently. Due to the age of the articles, it is not possible to compare the panels to raw data. The readers are asked to interpret the image with caution.&lt;/p&gt;&lt;p&gt;D’Alessio S, Margheri F, Serratì S, Pucci M (retired), Fibbi G (retired), and Del Rosso M (retired) agree with this Editorial Express of Concern.&lt;/p&gt;&lt;ol data-track-component=\"outbound reference\" data-track-context=\"references section\"&gt;&lt;li data-counter=\"1.\"&gt;&lt;p&gt;D’Alessio S, Fibbi G, Cinelli M, Guiducci S, Del Rosso A, Margheri F, Serratì S, Pucci M, Kahaleh B, Fan P, Annunziato F, Cosmi L, Liotta F, Matucci-Cerinic M, Rosso D, M. Matrix metalloproteinase 12–dependent cleavage of urokinase receptor in systemic sclerosis microvascular endothelial cells results in impaired angiogenesis. Arthr Rhuem. 2004;50:3275–85. https://doi.org/10.1002/art.20562.&lt;/p&gt;&lt;p&gt;Article CAS Google Scholar &lt;/p&gt;&lt;/li&gt;&lt;/ol&gt;&lt;p&gt;Download references&lt;svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"&gt;&lt;use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;/use&gt;&lt;/svg&gt;&lt;/p&gt;&lt;h3&gt;Authors and Affiliations&lt;/h3&gt;&lt;ol&gt;&lt;li&gt;&lt;p&gt;Department of Medical and Surgical Critical Care– DENOTHE, University of Florence, Florence, Italy&lt;/p&gt;&lt;p&gt;Betti Giusti, Luciana Rossi, Filippo Poggi, Ilaria Lapini, Alberto Magi, Gian Franco Gensini &amp; Rosanna Abbate&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Department of Experimental Pathology and Oncology– DENOTHE, University of Florence, Florence, Italy&lt;/p&gt;&lt;p&gt;Gabriella Fibbi, Francesca Margheri, Simona Serratì &amp; Mario Del Rosso&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Department of Internal Medicine, University of Florence, Florence, Italy&lt;/p&gt;&lt;p&gt;Angela Del Rosso, Marina Cinelli, Serena Guiducci &amp; Marco Matucci-Cerinic&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Division of Rheumatology, Medical College of Ohio, Toledo, OH, USA&lt;/p&gt;&lt;p&gt;Bashar Kahaleh&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Department of Internal Medicine, University of Pisa, Pisa, Italy&lt;/p&gt;&lt;p&gt;Laura Bazzichi &amp; Stefano Bombardieri&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Centro S Maria agli Ulivi, Fondazione Don Carlo Gnocchi, ONLUS IRCCS, Impruneta, Florence, Italy&lt;/p&gt;&lt;p&gt;Gian Franco Gensini&lt;/p&gt;&lt;/li&gt;&lt;/ol&gt;&lt;span&gt;Authors&lt;/span&gt;&lt;ol&gt;&lt;li&gt;&lt;span&gt;Betti Giusti&lt;/span&gt;View author publications&lt;p&gt;&lt;span&gt;You can also search for this author in&lt;/span&gt;&lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Gabriella Fibbi&lt;/span&gt;View author publications&lt;p&gt;&lt;span&gt;You can also search for this author in&lt;/span&gt;&lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Francesca Margheri&lt;/span&gt;View author publications&lt;p&gt;&lt;span&gt;You can also search for this author in&lt;/span&gt;&lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Simona Serratì","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"31 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736633","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}