Annals of the Rheumatic Diseases最新文献

{"title":"METTL1-mediated internal m⁷G methylation of cathepsin B mRNA promotes synovial aggression in rheumatoid arthritis.","authors":"Simin Chen, Kai Sun, Chenxi Peng, Yu Kuang, Shuoyang Zhang, Ruiru Li, Huijuan Hu, Suling Liu, Fan Su, Qian Qiu, Liuqin Liang, Ligang Jie, Youjun Xiao, Hanshi Xu","doi":"10.1016/j.ard.2025.09.010","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.010","url":null,"abstract":"<p><strong>Objectives: </strong>Recent studies show that methyltransferase-like 1 (METTL1)-mediated internal messenger ribonucleic acid (mRNA) N⁷-methylguanosine (m⁷G) modification has a unique role in cancer metastasis. Here, we aimed to uncover the role of METTL1-mediated internal mRNA m⁷G in controlling fibroblast-like synoviocytes' (FLSs') functions in rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>FLSs were separated from patients with active established RA. Western blot, immunohistochemistry, and immunofluorescence were used to measure protein expression in synovium. The Boyden chamber was used to detect cell migration and invasion. m⁷G RNA immunoprecipitation sequencing was performed to seek the potential target of METTL1. Dual-luciferase reporter gene assay was used to investigate the m⁷G-dependent regulation of cathepsin B (CTSB) by METTL1. The protein translation efficiency was detected by polysome profiling. METTL1 heterozygous knockout or intra-articular injection of METTL1 short hairpin ribonucleic acid adenovirus (Adv-shRNA-METTL1) was used to inhibit arthritis in RA models.</p><p><strong>Results: </strong>We observed increased levels of METTL1 and internal mRNA m⁷G in FLSs and synovial tissues from patients with RA. METTL1 knockdown or overexpression decreased or increased the migration and invasion of RA FLSs. Synovial METTL1 level was positively correlated with the disease activity score on 28 joints-erythrocyte sedimentation rate scores in patients with RA. METTL1 knockdown in vivo mitigated the severity of arthritis in RA animal models. Mechanistically, we probed that METTL1 promotes the aggressive action of RA FLSs through regulating the translation efficiency of the internal mRNA m⁷G modification of CTSB. CTSB knockdown also suppressed the aggression of RA FLSs.</p><p><strong>Conclusions: </strong>Our findings reveal an important role of METTL1-mediated internal mRNA m⁷G modification in promoting synovial aggression of RA, suggesting that METTL1 might be a potential target for therapy of RA, even other dysregulated FLS-associated diseases.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145353583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Teclistamab-induced rapid remission in refractory Anti-Jo-1 Antisynthetase Syndrome.","authors":"Elpida Phithak, Fredrik N Albach, Ioanna Minopoulou, Robert Biesen, Arnd Kleyer, Edgar Wiebe, Elise Siegert, Veronika Scholz, Marie Rehm, Qingyu Cheng, Arne Sattler, Stefano Bianco, Anja Fleischmann, Kay-Geert Hermann, Thula Walter-Rittel, Moritz Wagner, Jan Zernicke, Vincent Casteleyn, Martin Nielsen, Thomas Rose, Antonia Busse, Marie Luise Hütter-Krönke, Ulrich Keller, Udo Schneider, Leona Kawelke, Nikolas Ruffer, Werner Stenzel, Gerhard Krönke, David Simon, Tobias Alexander","doi":"10.1016/j.ard.2025.09.012","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.012","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145353586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blocking the neonatal Fc receptor as a novel approach to prevent cardiac neonatal lupus: a proof-of-concept study.","authors":"Philip M Carlucci, Mala Masson, Bettina F Cuneo, Justin S Brandt, Angus B Worthing, Peter Izmirly, Nicola Fraser, Nalani Sachan, Mary T Donofrio, Robert Clancy, Jill P Buyon","doi":"10.1016/j.ard.2025.09.011","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.011","url":null,"abstract":"<p><strong>Objectives: </strong>Novel biologic agents targeting the neonatal Fc receptor (FcRn) offer a promising strategy to prevent cardiac neonatal lupus (cardiac-NL) in pregnant patients with high-titre anti-SSA/Ro52 kD or 60 kD autoantibodies via dual effects: reducing serum immunoglobin G (IgG) levels and inhibiting placental transfer. This study was initiated to assess the feasibility of FcRn blockade as prophylactic therapy for recurrent cardiac-NL.</p><p><strong>Methods: </strong>A 34-year-old pregnant patient with systemic lupus erythematosus and 3 prior consecutive pregnancies complicated by neonatal lupus (1 cutaneous, 1 fatal cardiac-NL at 20 weeks, 1 cardiac-NL delivered at 32 weeks and neonatal cutaneous NL), each despite hydroxychloroquine 400 mg daily, was treated with weekly subcutaneous infusions of 560 mg rozanolixizumab (humanised IgG4 monoclonal antibody against FcRn) from gestational weeks 14 to 28 (to cover the vulnerable period of fetal cardiac injury) through a compassionate use designation. The patient performed home fetal heart rhythm monitoring thrice daily with weekly echocardiograms.</p><p><strong>Results: </strong>Maternal anti-SSA/Ro52 kD and 60 kD autoantibodies, total IgG, and subclasses IgG1, 2, 3 decreased by about 65% at gestational week 22, with a return to near baseline levels by week 34. The pregnancy was uncomplicated, resulting in a spontaneous vaginal delivery of a healthy neonate at 37 weeks. At delivery, cord blood and maternal IgG levels were normal, obviating the need for rescue intravenous immune globulin. The neonate had a normal echocardiogram and electrocardiogram but developed a rash consistent with neonatal lupus at 5 weeks of life. There were no serious adverse events.</p><p><strong>Conclusions: </strong>The successful application of FcRn blockade to prevent recurrent cardiac-NL sets a precedent for a multicentre study.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145328179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial profiling of giant cell arteritis tissues reveals immune heterogeneity and potential predictors of glucocorticoid response.","authors":"Cecilia Ansalone, Samuel McAllister, Ethan S Pickerill, Lin Zhang, David C Gemperline, Annie Peacock, Ishita Gupta, Dominic Mcgovern, Victoria Kellior, Evelyn Qian, Aysin Tulunay Virlan, Maria Laura Vieri, Holly Leslie, Yoana Doncheva, Claire Kennedy Dietrich, Sylvia Wright, Paul Cauchi, Timothy Beckman, Lisa Hutton, John Cole, Nigel B Jamieson, Isabella H Wulur, Ajay Nirula, Iain B McInnes, Robert J Benschop, Carl S Goodyear, Neil Basu","doi":"10.1016/j.ard.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.009","url":null,"abstract":"<p><strong>Objectives: </strong>Giant cell arteritis (GCA) is an immune-mediated vasculitis of large- and medium-sized arteries that can lead to systemic symptoms and irreversible vision loss. Glucocorticoids (GCs) remain the primary treatment but fail to induce sustained remission (SR) in approximately half of patients, resulting in disease relapses and significant treatment-related toxicity. We aimed to identify tissue-based markers at disease onset capable of distinguishing patients who later achieve SR from those who do not (non-remission [NR]) under GC monotherapy.</p><p><strong>Methods: </strong>Using spatial biology techniques, we performed a comprehensive analysis of GCA-affected arterial tissues obtained at disease onset, correlating molecular profiles with clinical trajectory. We compared gene expression and immune cell populations between SR and NR groups, corroborated key findings by immunohistochemistry, and evaluated the diagnostic performance of identified biomarkers.</p><p><strong>Results: </strong>Patients with NR exhibited an upregulation of extracellular matrix remodelling (ECM) and T cell activation pathways, reflecting persistent inflammation and fibrotic-like responses. By contrast, SR cases were distinguished by an enrichment of immunoglobulin G-producing plasma cells in the adventitia, which correlated with increased macrophage infiltration in the intima. Quantitative analyses suggested that combining plasma cell and macrophage markers could accurately predict GC responsiveness.</p><p><strong>Conclusions: </strong>Our findings reveal an immunopathologic signature in GCA at diagnosis, characterised by plasma cell-rich infiltrates associated with favourable outcomes, and ECM- and T cell-associated inflammation enriched in GC-refractory cases. These insights could foster a precision medicine approach to GCA management, enabling patient stratification for GC-sparing therapies and optimising patient outcomes.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deconstruction of tophi and synovium defines SPP1⁺ macrophages involved in extracellular matrix remodelling in gout.","authors":"Hanlin Xu, Zhechen Liu, Xiaofeng Zhou, Xiaoxi Ji, Xingwang Liu, Xiaoxia Zhu, Liwei Lu, Nicola Dalbeth, Rui He, Yinghui Hua","doi":"10.1016/j.ard.2025.09.003","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.003","url":null,"abstract":"<p><strong>Objectives: </strong>Gout is a prevalent condition characterised by high serum urate levels, leading to crystal deposition in the joints. Although many studies have explored the mechanisms underlying gout flares, the dynamics of tophus formation remain unknown. This study provides the first transcriptomic profile of the tophaceous gout joint and investigates immune-stromal cell interactions in the pathogenesis of tophus formation.</p><p><strong>Methods: </strong>Single-cell transcriptomic profiling was conducted on 44,221 synovial tissue cells from patients with intercritical gout (without tophi) and tophaceous gout. Spatial transcriptomics showed gene expression patterns in the corona and fibrovascular zones of tophi. Gene expression pattern comparisons, pseudotime, and differential gene enrichment analyses were conducted on stage-specific macrophage subsets. Immunofluorescence and flow cytometry on the tophi samples validated the transcription results and visualised the spatial localisation of the macrophage-fibroblast subpopulation. Differential causal inference combined with Mendelian randomisation elucidated gene regulatory networks and their causal relationships with gout pathology.</p><p><strong>Results: </strong>We identified SPP1⁺/MMP9^+/CHI3L1⁺ macrophages within the corona zone exclusive to tophaceous gout, exhibiting extracellular matrix regulation genes, enhanced integrin-mediated interactions with stromal cells and transitional potential towards osteoclast differentiation. Notably, coexpression of the fibroblast marker S100A4 and COL6A2 in these macrophages suggested a fibroblast-like phenotype. Distinct CD4⁺ T-cell transcriptional profiles between disease states indicated a phenotypic shift from inflammatory to immune-regulatory subsets during tophus development.</p><p><strong>Conclusions: </strong>This study reveals a novel macrophage population (SPP1⁺/MMP9^+/CHI3L1⁺) with dual immunomodulatory and matrix-remodelling capabilities, exclusively present in tophus tissues but absent in intercritical gout synovium or flare-associated synovial fluid. It may play a role in the pathogenesis of fibrosis and bone erosion in gout.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EULAR recommendations for the management of systemic lupus erythematosus with kidney involvement: 2025 update.","authors":"Antonis Fanouriakis, Myrto Kostopoulou, Hans-Joachim Anders, Jeanette Andersen, Martin Aringer, Michael W Beresford, Andrea Doria, Eleni Frangou, Richard Furie, Dafna D Gladman, Frederic Houssiau, Alexandre Karras, Marios Kouloumas, Anastasia-Vasiliki Madenidou, Ana Malvar, Smaragdi Marinaki, Chi Chiu Mok, Gabriella Moroni, Ioannis Parodis, Simona Rednic, Cristiana Sieiro Santos, Carlo Alberto Scire, Josef S Smolen, Farah Tamirou, Yoshiya Tanaka, Y K Onno Teng, Elisabet Welin, George Bertsias, Dimitrios T Boumpas","doi":"10.1016/j.ard.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.007","url":null,"abstract":"<p><strong>Objectives: </strong>The objective of this study was to update the 2019 European Alliance of Associations for Rheumatology (EULAR)/ European Renal Association/European Dialysis Transplantation Association (ERA-EDTA) recommendations for the management of systemic lupus erythematosus (SLE) with kidney involvement, taking into consideration emerging evidence and recent developments in the field.</p><p><strong>Methods: </strong>We recruited an international Task Force of experts and followed the EULAR standard operating procedures. We performed systematic literature research (period January 2019 to March 2024), followed by the modified Delphi method, to form questions, elicit expert opinions, and reach consensus. The new evidence was examined, taking into consideration previous updates.</p><p><strong>Results: </strong>The Task Force agreed on 4 overarching principles and 13 recommendations, which were also evaluated for their feasibility and impact on clinical care. These concern the use of kidney biopsy for diagnosis; targets of therapy and treatment milestones; immunomodulatory therapy with antimalarials, glucocorticoids, immunosuppressives (mycophenolate, cyclophosphamide, and calcineurin inhibitors), and biologics (belimumab, obinutuzumab, and rituximab); nonimmune therapy (kidney protection, vaccinations, cardiovascular, and bone protection); family planning; and management of kidney failure. Guidance on single-agent or early combination immune therapy, glucocorticoid tapering and withdrawal, duration of immune therapy, and treatment of refractory disease is provided.</p><p><strong>Conclusions: </strong>The updated EULAR recommendations provide evidence- and expert-based consensus on the management of SLE with kidney involvement, adjusted for severity, and taking into consideration long-term efficacy, safety, cost, and local availability of drugs.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Entheseal tissue signature in response to IL-17A inhibition in psoriatic arthritis: results from the EBIO entheseal biopsy study.","authors":"Maria Gabriella Raimondo, Hashem Mohammadian, Simon Rauber, Stefano Alivernini, Vladyslav Fedorchenko, Aleix Rius Rigau, Mario Raphael Angeli, Filippo Fagni, Giulia Corte, Koray Tascilar, Hannah Labinsky, Alina M Ramming, Frank Roemer, Juergen Rech, Lars Braeuer, Maria Antonietta D'Agostino, Georg Schett, Milena Pachowsky, Arnd Kleyer, Andreas Ramming","doi":"10.1016/j.ard.2025.08.032","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.032","url":null,"abstract":"<p><strong>Objectives: </strong>Enthesitis, a hallmark of psoriatic arthritis (PsA), reflects the interplay between mechanical stress and immune dysregulation at tendon-bone interfaces. This study investigates the cellular and molecular responses in entheseal tissues following interleukin (IL)-17A inhibition in patients with active PsA.</p><p><strong>Methods: </strong>In this prospective, interventional phase 4 trial, we enrolled 10 patients with enthesitis of the lateral epicondyle, performed entheseal biopsies, and analysed tissues by imaging mass cytometry (IMC) and spatial transcriptomics before and after treatment.</p><p><strong>Results: </strong>Following 24 weeks of IL-17A inhibition, 9/10 patients of the cohort clinically responded to treatment as assessed by Disease Activity in Psoriatic Arthritis (DAPSA), Spondyloarthritis research consortium of canada (SPARCC) score, and power Doppler sonography. IMC analysis showed significant reductions of enthesitis-related immune cell populations, in particular IL-17-producing CD4, CD8, CD4^neg/CD8^neg T cells, granulocytes, and innate lymphoid cells type 3. Spatial transcriptomics revealed that CD200+DKK3+ fibroblasts and innate lymphoid cells type 2 expanded and formed an anti-inflammatory niche upon treatment. Notably, IL-17A inhibition led to decreased osteoblast differentiation markers, suggesting a potential mechanism to inhibit pathological bone formation.</p><p><strong>Conclusions: </strong>These findings underline the pivotal role of IL-17A in enthesitis, showing that IL-17A inhibition profoundly modulates the tissue microenvironment of entheses in PsA.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the immunopathophysiology of polymyalgia rheumatica: implications for treatment.","authors":"Ernest H Choy, Sebastian H Unizony, Alvin F Wells, Bhaskar Dasgupta, Frank Buttgereit, Yoshiya Tanaka","doi":"10.1016/j.ard.2025.09.005","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.005","url":null,"abstract":"<p><p>Polymyalgia rheumatica (PMR) is one of the most common inflammatory rheumatic diseases in people aged ≥50 years and is characterised by neck pain, bilateral shoulder and hip girdle pain, and morning stiffness. It is closely interlinked with giant cell arteritis (GCA) (potentially considered the GCA-PMR spectrum) and rheumatoid arthritis and shares a common immunopathophysiology with both. Glucocorticoids (GCs) have been the standard of care for PMR for several decades (American College of Rheumatology/European Alliance of Associations for Rheumatology guidelines); however, >50% of patients cannot successfully taper GCs, and long-term treatment is associated with considerable GC-related adverse events. Immunohistological studies using biopsies from subacromial bursae have indicated that various cytokines and cells, including macrophages, interleukin-6 (IL-6), and fibroblast-like synoviocytes (FLS), play an integral role in the immunopathophysiology of PMR. Proinflammatory cytokines, including IL-1, IL-6, IL-17, and tumour necrosis factor-alpha, activate FLS which then secrete IL-6 that can further promote FLS proliferation. Activation of synoviocytes in bursae may result in bursitis which can lead to a high concentration of acute-phase reactants and systemic inflammation. IL-6 also plays a role in sleep disturbances, mood disorders, pain, and fatigue; it is often seen in PMR, via disruption of the hypothalamic-pituitary-adrenal axis, and actions on the peripheral and central pain pathways. Given the diverse roles of IL-6 in the immunopathophysiology of PMR, targeted molecular therapies such as IL-6 receptor inhibitors offer promising alternatives for disease management, distinct from the nonspecific immunosuppressive effects of GCs. In this review, we describe the immunopathophysiology of PMR and discuss unmet medical needs and therapeutic options for PMR.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence on 'ERS/EULAR clinical practice guidelines for connective tissue disease-associated interstitial lung disease' by Antoniou et al.","authors":"Salman Afaq Zarar, Bjørg-Tilde Svanes Fevang, Christian Lillebø Alsing, Eirik Ikdahl","doi":"10.1016/j.ard.2025.09.006","DOIUrl":"https://doi.org/10.1016/j.ard.2025.09.006","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What lies beneath early-onset disc degeneration?","authors":"Haijun Tian, Baozhi Ding, Zeming Zeng, Shichang Zhao, Jie Zhao","doi":"10.1016/j.ard.2025.08.025","DOIUrl":"https://doi.org/10.1016/j.ard.2025.08.025","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.6,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}