Journal of Inflammation Research最新文献

{"title":"Tocilizumab for Non-Infectious Uveitis: A Systematic Review.","authors":"Haixing Cao, Kaiyu Bian, Cong Ma, Naiwen Zhang, Xiang Ma","doi":"10.2147/JIR.S533011","DOIUrl":"10.2147/JIR.S533011","url":null,"abstract":"<p><p>Non-infectious uveitis (NIU) comprises a heterogeneous group of diseases causing severe ocular inflammation that threatens vision. In addition to visual impairment, patients frequently endure chronic pain, functional disorders, and psychosocial stress, all of which substantially reduce quality of life. Treating NIU remains challenging because many patients respond inadequately to high-dose corticosteroids and various immunosuppressants. This systematic review evaluated the efficacy and safety of tocilizumab (TCZ) in NIU treatment by analyzing case reports and small-scale studies. A systematic search of PubMed, Web of Science, and Embase up to May 1, 2025, identified all published cases reporting baseline and follow-up visual acuity alongside intervention details. The Newcastle-Ottawa Scale (NOS) assessed methodological quality, while the Joanna Briggs Institute (JBI) tool evaluated risk of bias. The systematic review included 96 patients (36 males, 60 females) with an average age of 35 years (range 4-72). Behçet's disease (BD) represented the most common underlying condition (33 cases), and panuveitis was the primary anatomical subtype (35 cases). Prior to TCZ initiation, patients had received an average of 2.8 conventional immunosuppressants and 1.6 biologics, yet persistent disease activity remained. The median interval from diagnosis to TCZ treatment was 11.8 months (range 4-24). Following TCZ administration, vision improved in 62.5% of patients, intraocular inflammation was controlled in 83.3%, and macular edema resolved in 90.9%. Overall, 83.3% (80/96) responded favorably to TCZ. These findings indicate that TCZ may serve as an effective alternative for managing refractory NIU when other treatments fail.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13117-13138"},"PeriodicalIF":4.1,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"lncRNA RNA AC114812 Regulates the Inflammatory Response of Periodontal Ligament Cells via the miR-181a-5p-SPP1 Axis.","authors":"Tong Tong, Fei Zhao, Ran Tao, Chunyan Liu, Bing Liu","doi":"10.2147/JIR.S534691","DOIUrl":"10.2147/JIR.S534691","url":null,"abstract":"<p><strong>Background: </strong>Long noncoding RNAs (lncRNAs) play a significant role in the occurrence and development of periodontitis. We investigate the potential role of the lncRNA AC114812 in the lipopolysaccharide (LPS) induced proliferation, migration and inflammatory response of periodontal ligament cells (PDLCs) via the miR-181a-5p-SPP1 axis.</p><p><strong>Methods: </strong>Bioinformatics analysis and whole transcriptome sequencing analysis were conducted on the gingival tissues of three pairs of healthy and periodontitis patients to screen out lncRNAs with differential expression in periodontitis and a periodontitis cell model was constructed via stimulation with LPS. The expression levels of the lncRNA AC114812 in tissues and cells were detected via real-time quantitative polymerase chain reaction (qRT-PCR), and the expression localization was detected via fluorescence in situ hybridization (FISH). The role of si-AC114812 in periodontitis was investigated through qRT-PCR, MTT assay and wound healing experiments. Through database screening combined with sequencing results, the competitive endogenous RNA (ceRNA) mechanism of lncRNA AC114812-miR-181a-5p-SPP1 was verified via a dual-luciferase gene reporter assay.</p><p><strong>Results: </strong>LncRNA AC114812 was highly expressed in periodontitis tissues. Knockdown of lncRNA AC114812 inhibited the expression of inflammatory factors interleukin-1β (IL-1β) and interleukin-6 (IL-6) in PDLCs stimulated by inflammation and improved the proliferation and migration abilities of PDLCs affected by inflammation. FISH assays confirmed that the lncRNA AC114812 was expressed mainly in cytoplasm and may have a sponge effect. The ceRNA mechanism of the lncRNA AC114812-miR-181a-5p-SPP1 was predicted. The dual-luciferase gene reporter assay verified the existence of binding sites among the three genes and their mutual regulatory effects.</p><p><strong>Conclusion: </strong>By regulating the expression of long non-coding RNA AC114812, the inflammatory response can be alleviated, thereby affecting cell proliferation and migration. The effect may be achieved through the miR-181a-5p-SPP1 axis. These can provide new strategies and intervention targets for the prevention and treatment of periodontal diseases.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13039-13053"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine Learning and Mendelian Randomization Identify Six Cell Death-Related Genes Driving Ulcerative Colitis Progression and Treatment Response.","authors":"Longfei Dai, Weiguo Zhou, Along Li, Xinjian Xu, Bin Yuan, Zhen Zhang","doi":"10.2147/JIR.S536145","DOIUrl":"10.2147/JIR.S536145","url":null,"abstract":"<p><strong>Background: </strong>The pathogenesis of ulcerative colitis (UC) is thought to involve abnormal regulation of cell death. However, key cell death-related genes (CDGs) that drive disease progression have not been fully characterized. The identification of these CDGs is thought to potentially reveal new therapeutic targets.</p><p><strong>Methods: </strong>Machine learning (ML) and Mendelian randomization (MR) methods were integrated to identify CDGs with causal effects in UC progression. The validation included immune-related analysis, drug response assessment (infliximab/vedolizumab/golimumab), patient stratification based on consensus clustering, and functional validation.</p><p><strong>Results: </strong>Six key CDG genes (<i>VNN1, PTGDS, MMP9, IL13RA2, S100A8</i>, and <i>IL1B</i>) were identified by ML. VNN1 and MMP9 were confirmed by MR to be pathogenic risk factors for UC progression. All six genes were significantly associated with immune cell infiltration, pro-inflammatory cytokines, and intestinal barrier dysfunction. Compared with non-responders, the expression of these six CDGs was significantly downregulated in biologic therapy responders. Based on these genes, patients with UC were classified into two groups: the C1 group with severe disease activity and the C2 group with reduced Mayo scores and enhanced treatment sensitivity. Additionally, knocking down VNN1 functionally alleviated intestinal inflammation.</p><p><strong>Conclusion: </strong>These six genes can be used to assess the severity of UC and predict treatment outcomes.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13073-13088"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The m⁶A Modification in T Helper Cells Regulates the Pathogenesis of Autoimmune Diseases.","authors":"Qi Jiang, Xin Wang, Yingping Wu, Dawei Cui","doi":"10.2147/JIR.S537243","DOIUrl":"10.2147/JIR.S537243","url":null,"abstract":"<p><p>The pathogenesis of autoimmune diseases remains unclear, which is associated with T helper (Th) cell subsets such as Th1, Th2, Treg and Tfh cells. Recent studies have indicated the involvement of N⁶-methyladenosine (m⁶A) modification in the pathogenesis of autoimmune diseases, and m⁶A also affects the differentiation, and function of Th cells. However, few reports focused on the relationship between m⁶A modification in Th cell subsets and autoimmune diseases. This review summarizes the latest research progress on m⁶A modification in common autoimmune diseases, specifically highlighting how various m⁶A-modifying enzymes influence the differentiation and function of Th cells and disease progression. Elucidating the relationship between m⁶A modification and Th cells in autoimmune diseases may provide a new perspective for disease prevention and targeted therapy. Finally, this review also elaborates on the impact of m⁶A on the clinical diagnosis and treatment of autoimmune diseases, as well as the challenges that need to be addressed.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13159-13172"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influenza A (H1N1) and COVID-19 Pneumonias: An Evaluation in the Light of New Hematologic Indices.","authors":"Mihrican Yeşildağ, Rahim Kocabas","doi":"10.2147/JIR.S545387","DOIUrl":"10.2147/JIR.S545387","url":null,"abstract":"<p><strong>Objective: </strong>Influenza A (H1N1) and COVID-19 viruses are two very different airway viral pneumonia agents that cause similar clinical manifestations and coinfections. The aim of this study was to investigate new laboratory indices, clinical and radiological findings that may help in the differential diagnosis of these two viral pneumonias.</p><p><strong>Material and methods: </strong>Eighty-nine hospitalized patients, 38 with Influenza A (H1N1) and 51 with COVID-19 pneumonia, were retrospectively analyzed. Laboratory parameters, clinical, and radiological findings of the patients were obtained from their medical files. Numerous hematological and biochemical parameters (neutrophil, monocytes, mean corpuscular volume (MCV), albumin, uric acid, etc) were investigated and new indices (neutrophil/albumin ratio (NAR), lymphocyte-monocyte ratio (LMR), etc) were calculated. Both viral pneumonias were compared in terms of new hematological and biochemical indices and clinical and radiological outcomes.</p><p><strong>Results: </strong>In terms of clinical symptoms, fever, cough, and shortness of breath were higher in influenza A (H1N1) pneumonia, while sore throat, headache, and malaise were higher in COVID-19 pneumonia. Consolidations in influenza A (H1N1) pneumonia and round ground-glass opacities in COVID-19 pneumonia were found as typical radiologic findings. The laboratory parameters most associated with COVID-19 pneumonia were monocytes (OR 27.327, %95 CI: 4.143-180.234, p=0.001), MCV (OR 1.130, %95 CI:1.011-1.262, p=0.031), albumin (OR 0.314, %95 CI:0.111-0.888, p=0.029) and uric acid (OR 1.631, %95 CI:1.055-2.522, p=0.028), and laboratory indices were LMR (OR 0.677, %95 CI:0.492-0.933, p=0.017) and NAR (OR 1.514, %95 CI:1.004-2.282, p=0.048).</p><p><strong>Conclusion: </strong>The most significant laboratory parameters predictive of COVID-19 pneumonia were monocytes, uric acid, albumin, and MCV and the most effective indices were LMR and NAR. Round ground glass opacities were the primary radiological findings suggestive of COVID-19 pneumonia.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13103-13116"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Druggable Targets for Pelvic Inflammatory Disease: Mendelian Randomization and Experimental Validation.","authors":"Chunxiao Dang, Qing Wu, Jing Pan, Xiao Yu, Jinxing Liu, Pengfei Liu, Yayu Wang","doi":"10.2147/JIR.S530521","DOIUrl":"10.2147/JIR.S530521","url":null,"abstract":"<p><strong>Background: </strong>Pelvic inflammatory disease (PID) is a common gynecological disorder that seriously affects women's physical and mental health, yet there are few effective therapeutic options.</p><p><strong>Objective: </strong>Mendelian randomization (MR) has been used to repurpose existing drugs and identify new therapeutic targets. Therefore, we performed a systematic drugable genome-wide MR analysis to explore potential therapeutic targets for PID.</p><p><strong>Methods: </strong>We utilized cis-expressed quantitative trait loci (cis-eQTL) of druggable genes and PID Genome-Wide Association Study (GWAS) data to perform MR analysis and colocalization analysis, screened candidate drugs through drug prediction, identified the most stable druggable genes with the highest binding affinity through molecular docking, and finally constructed a PID rat model to validate gene expression.</p><p><strong>Results: </strong>MR analysis, colocalization analysis, and protein interaction analysis identified six key genes. Drug enrichment analysis and molecular docking revealed two potential drugs (Sunitinib and Everolimus) targeting Albumin (ALB), Interleukin 6 (IL6), and Cluster of Differentiation 4 (CD4). In the PID rat model, ALB and IL6 expression decreased, while CD4 expression increased.</p><p><strong>Conclusion: </strong>Our MR analysis provides genetic evidence supporting ALB, IL6, and CD4 as druggable genes for PID treatment. Among the drug candidates with repurposing opportunities targeting the above genes, Sunitinib and Everolimus were effective. Subsequent in vivo experiments validated the differential expression of ALB, IL6, and CD4 in PID rats.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13089-13101"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.","authors":"Shanshan Tang, Yuting Sun, Wenjie Sun, Xiaomin Kang, Xuefei Zhao, Linlin Jiang, Qing Gao, Xuedong An, Hangyu Ji, Fengmei Lian","doi":"10.2147/JIR.S545938","DOIUrl":"10.2147/JIR.S545938","url":null,"abstract":"<p><p>The escalating incidence and mortality of diabetic kidney disease (DKD) underscore the critical need to elucidate its pathogenesis. Programmed cell death (PCD) plays a dual role in maintaining physiological homeostasis and driving pathological processes in DKD. Accumulating evidence demonstrates that apoptosis, autophagy, pyroptosis, and ferroptosis contribute directly or indirectly to DKD progression via distinct gene-regulated signaling pathways. Recently identified PCD modes (eg, necroptosis, parthanatos) remain poorly characterized in DKD, with emerging evidence suggesting crosstalk between different PCD pathways. This review synthesizes current knowledge on PCD-mediated DKD pathogenesis and PCD-targeted therapies, while highlighting research limitations (eg, unclear PCD interactions, translational gaps). We propose that dissecting the multifaceted roles of PCD in DKD will deepen mechanistic understanding and accelerate the development of novel therapeutics, offering significant scientific and clinical benefits.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13001-13037"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Value of Lymphocyte Count in Risk Prediction of Papillary Thyroid Carcinoma: A Case-Control Study in a Chinese Population.","authors":"Xiu-Ping Qiu, Ru-Ying Xie, Yang Chen, Mei Tu, Ting Wang","doi":"10.2147/JIR.S528176","DOIUrl":"10.2147/JIR.S528176","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the association between preoperative peripheral blood lymphocyte count and the risk of papillary thyroid carcinoma (PTC) in a Chinese population using a case-control design.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on 1832 patients who underwent thyroid surgery, including 1007 diagnosed with benign thyroid nodules and 825 with PTC. Clinical parameters, including lymphocyte count, nodule volume, thyroid function, and thyroid autoantibody levels, were assessed. Multivariate regression and stratified analyses were conducted to examine the relationship between lymphocyte count and PTC risk.</p><p><strong>Results: </strong>The mean lymphocyte count was significantly higher in patients with PTC compared to those with benign thyroid nodules (1.20 ± 0.63 vs 1.87 ± 0.53, <i>p</i> < 0.001). Multivariate regression analysis indicated a dose-response relationship, with patients in the highest lymphocyte count group exhibiting an odds ratio of 15.02 (95% CI: 7.52-30.03, <i>p</i> < 0.0001). Receiver operating curve analysis demonstrated good diagnostic performance (AUC = 0.8068). Stratified analyses revealed variations in risk patterns across subgroups stratified by age, sex, and nodule volume.</p><p><strong>Conclusion: </strong>Lymphocyte count may serve as a potential predictor of PTC risk. This finding may provide new insights into early clinical risk stratification and personalized screening strategies in the management of PTC.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12971-12988"},"PeriodicalIF":4.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Core SASP-Related Genes TGFBI and ANXA6 for Diagnosing Ulcerative Colitis-Related Colorectal Cancer Through Machine Learning.","authors":"Jukun Zhang, Ping Wang, Siqi Yuan, Yingjian Zhang","doi":"10.2147/JIR.S538960","DOIUrl":"10.2147/JIR.S538960","url":null,"abstract":"<p><strong>Purpose: </strong>To explore the role of senescence-associated secretory phenotype (SASP) in ulcerative colitis-related colorectal cancer (UCRCC) precision diagnosis and pathogenesis.</p><p><strong>Methods: </strong>In this study, we first screened the SASP-related genes (SASPRGs) in the ulcerative colitis (UC) and colorectal cancer (CRC) datasets using differentially expressed genes (DEGs) and weighted gene co-expression network analysis (WGCNA). Subsequently, the core SASPRGs were further identified using 113 combinations of 10 machine learning algorithms, and evaluating their expression levels, diagnostic efficacy, prognostic value, and relationship with immune cells. Expression patterns of core SASPRGs were analyzed using scRNA-seq, and a molecular regulatory network was constructed. In addition, immunotherapy response and drug sensitivity analysis were conducted to screen therapeutic drugs targeting core SASPRGs. Finally, their expression levels were validated through in vivo experiments.</p><p><strong>Results: </strong>We identified 12 core SASPRGs, among which TGFBI and ANXA6 exhibited satisfactory diagnostic efficacy and prognostic value for UC and CRC. ANXA6 and TGFBI are highly expressed in monocytes and fibroblasts, and are associated with the infiltration of multiple immune cells. In addition, high TGFBI and ANXA6 groups showed poor responses to immunotherapy. The candidate therapeutic drugs screened by drug sensitivity analysis showed good binding ability with ANXA6 and TGFBI. Finally, the expression levels of TGFBI and ANXA6 were significantly increased in UC and CRC mouse models.</p><p><strong>Conclusion: </strong>Overall, TGFBI and ANXA6 are crucial in UCRCC, serving as novel diagnostic markers. They exhibit robust predictive capabilities on patient prognosis and immunotherapy response, offering actionable insights to optimize therapeutic decision-making and advance personalized treatment paradigms in UCRCC management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12909-12928"},"PeriodicalIF":4.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of IL-20RA in Cerebrospinal Fluid Associated with the Risk of Moyamoya Disease: A Molecular Signatures Analysis with an Inflammation Proteomics Landscape.","authors":"Chengdong Xia, Bohang Liu, Yangchun Hu, Hongwei Cheng, Lei Ye","doi":"10.2147/JIR.S545941","DOIUrl":"10.2147/JIR.S545941","url":null,"abstract":"<p><strong>Purpose: </strong>Moyamoya disease (MMD) is a cerebrovascular disorder with diverse clinical manifestations. Surgical revascularization is currently the optimal choice in the treatment of MMD; however, it could not prevent the progression of the disease. Inflammation and immunity factors have been reported to play the pivotal role in the pathogenesis of MMD, but there were still limited studies concerning the inflammatory landscape. Here, we aimed to investigate the molecular signatures of MMD to outline the inflammatory feature of MMD.</p><p><strong>Patients and methods: </strong>A total of 89 MMD patients and 93 healthy subjects were recruited for this study. We then divided all patients into screening cohort (15 MMD patients and 21 healthy subjects) and validation cohort (74 MMD patients and 72 healthy subjects). Proteomic analysis of the cerebrospinal fluid (CSF) was performed in the screening cohort, which contained 363 inflammation-related molecules. Then we used ELISA assay to validation of molecules of differential expression.</p><p><strong>Results: </strong>We screened 192 inflammation-related proteins that were differentially expressed in the CSF of MMD patients. Among that, 191 proteins were upregulated, while IL-20RA were downregulated (p=0.042). The bioinformatic analysis found a potential inflammatory landscape of MMD, offering clues for pathogenetic and therapeutic targets in the mechanistic study. We then validated that downregulation of IL-20RA in CSF was associated with the risk of MMD in the validation cohort.</p><p><strong>Conclusion: </strong>This study provided molecular signatures of MMD with a large-scale proteomic analysis of CSF. IL-20RA might be a key element in the pathogenesis of MMD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12961-12970"},"PeriodicalIF":4.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12453043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}