Inflammation Research最新文献_第5页

Histamine H₃ receptor: an emerging target for cancer therapy? 组胺H3受体：癌症治疗的新靶点？

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02054-z

Paolo Lauretta, Rocio Martinez Vivot, Agueda Velazco, Vanina A Medina

引用次数: 0

Intestinal NF-κB pathway-mediated pyroptosis contributes to endotoxemia-induced intestinal injury. 肠道NF-κB通路介导的焦亡参与内毒素血症诱导的肠道损伤。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02064-x

Xinrui Wang, Wen Lu, Ruibin Cai, Jie Jiang, Chuyue Wang, Jinli Liao, Yongshu Zhang, Danni Li, Zi Ye, Ming Long, Zhihao Liu

{"title":"Intestinal NF-κB pathway-mediated pyroptosis contributes to endotoxemia-induced intestinal injury.","authors":"Xinrui Wang, Wen Lu, Ruibin Cai, Jie Jiang, Chuyue Wang, Jinli Liao, Yongshu Zhang, Danni Li, Zi Ye, Ming Long, Zhihao Liu","doi":"10.1007/s00011-025-02064-x","DOIUrl":"https://doi.org/10.1007/s00011-025-02064-x","url":null,"abstract":"Pyroptosis contributes to activation of the innate immunity system and defense against infection by pathogens. Endotoxemia is the host inflammatory storm occurring in response to severe and life-threatening infections caused by endotoxin from gram-negative bacilli. However, whether pyroptosis is involved in intestinal epithelial cell (IEC) or intestinal stem cell (ISC) injury induced by endotoxemia remains unclear. Mice with NF-κB p65 deletion in IECs (p65IEC - KO) were used to investigate the role of NF-κB-mediated pyroptosis in endotoxemia-induced intestinal injury. Morphology, pyroptosis, permeability, inflammation, endoplasmic reticulum stress in the intestine and survival were evaluated in WT and p65IEC - KO mice. Pyroptosis was found in intestinal epithelial cells of mice treated with lipopolysaccharide (LPS), but was significantly reduced in p65IEC - KO mice. Mice with endotoxemia exhibited morphological alterations in intestinal tissue, with a shortened villus length and crypt depth, increased intestinal permeability, increased inflammatory factors, and reduced survival rate, all of which were markedly improved in p65IEC - KO mice. Importantly, ER stress was found to be downregulated in IECs of p65IEC - KO mice with endotoxemia. Furthermore, the ER stress activator tunicamycin markedly enhanced IEC pyroptosis and aggravated intestinal injury in p65IEC - KO mice with endotoxemia. NF-κB p65-mediated pyroptosis participates in IEC injury in response to endotoxemia via regulation of ER stress. It may provide a potential therapeutic target for protecting against endotoxemia-induced intestinal injury.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"94"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lipid metabolic adaptations during inflammation are controlled by the circadian clock and impaired by light at night. 炎症期间的脂质代谢适应是由生物钟控制的，并受到夜间光线的损害。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02066-9

Beata Benedikova, Viera Sebenova Jerigova, Michal Zeman, Monika Okuliarova

{"title":"Lipid metabolic adaptations during inflammation are controlled by the circadian clock and impaired by light at night.","authors":"Beata Benedikova, Viera Sebenova Jerigova, Michal Zeman, Monika Okuliarova","doi":"10.1007/s00011-025-02066-9","DOIUrl":"10.1007/s00011-025-02066-9","url":null,"abstract":"Objective and design: Immune defence requires systemic metabolic changes to redirect energy and nutrients to activated immune cells. The circadian clock is known to control the immune response, but its role in regulating metabolic adaptations following the immune challenge remains poorly understood. We aimed to examine the inflammatory and metabolic responses in rat liver and visceral white adipose tissue (vWAT) after time-of-day-dependent endotoxin stimulation under a regular light/dark cycle or dim artificial light at night (ALAN; ~2 lx), which disrupts immune and metabolic rhythms. Male rats were challenged with lipopolysaccharide (LPS) either during the day or night and acute changes in metabolic pathways and the peripheral metabolic clocks were analysed at both systemic and molecular levels.Results: In the control light/dark cycle, we observed higher fatty acid (FA) mobilization in vWAT after daytime than nighttime LPS injection. Similarly, hepatic glucose metabolism was more responsive to daytime than nighttime LPS, while the opposite trend was observed for FA uptake and synthesis. This daily variability in metabolic changes was associated with the inflammatory response, involving nuclear factor interleukin-3 regulated (NFIL3) in the liver and nuclear factor-kappa B (NF-κB)/NLR family, pyrin domain containing 3 (NLRP3) inflammasome pathway in vWAT. Hepatic and adipose clocks also showed time-of-day-dependent response to LPS, indicating a direct link to circadian regulation. Disruption of metabolic clocks by ALAN impaired the capacity of rats to maintain lipid metabolic adaptations during inflammation.Conclusions: Together, our results highlight the role of circadian clocks in LPS-induced responses of glucose and FA metabolism and their susceptibility to disruption by ALAN.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"96"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12206677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The complement system in autoimmune diseases: pathogenesis, diagnostic markers, and therapeutic strategies. 自身免疫性疾病中的补体系统：发病机制、诊断标记和治疗策略。

IF 5.4 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02061-0

Yanan Gao, Liangyu Mi, Ke Xu

{"title":"The complement system in autoimmune diseases: pathogenesis, diagnostic markers, and therapeutic strategies.","authors":"Yanan Gao, Liangyu Mi, Ke Xu","doi":"10.1007/s00011-025-02061-0","DOIUrl":"10.1007/s00011-025-02061-0","url":null,"abstract":"Objective: Autoimmune diseases (AIDs) are a spectrum of chronic conditions characterized by abnormal immune responses directed against the body's own tissues. Current therapeutic strategies still rely on broad-spectrum immunosuppression, which often produces severe adverse effects and is ineffective in targeting comorbidities. The complement system, a key component of innate immunity, has been increasingly recognized for its role in the pathogenesis and progression of AIDs. This review aims to assess the diagnostic and therapeutic potential of targeting the complement system in AIDs.Methods: A comprehensive literature review was conducted using the PubMed, Medscape, and ClinicalTrials.gov databases. The analysis included both original research and review articles, as well as data from ongoing and completed clinical trials focused on complement-targeted therapies.Results: Complement activation contributes to inflammation, tissue injury, and amplification of adaptive immunity in AIDs. Current and emerging complement-targeted therapies, including monoclonal antibodies and small-molecule inhibitors has shown promising preliminary outcomes in reducing disease activity with fewer adverse effects.Conclusion: Targeting the complement system represents a promising and more precise strategy for the treatment of AIDs. Ongoing clinical evaluation is essential to establish its long-term safety and efficacy, with the potential to significantly advance future therapeutic approaches.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"93"},"PeriodicalIF":5.4,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aryl hydrocarbon receptor (AhR) alleviates the LPS-induced inflammatory responses in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy. 芳烃受体（Aryl hydrocarbon receptor, AhR）通过激活PINK1/ parkinson介导的线粒体自噬，缓解lps诱导的IPEC-J2细胞炎症反应。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02063-y

Mengfei Ma, Jianxun Guo, Xiaoying Su, Baocai Ma, Xiufen Wang, Mingyu Wangshao, Kai Zhong, Yueying Wang, Guoyu Yang, Yingqian Han

{"title":"Aryl hydrocarbon receptor (AhR) alleviates the LPS-induced inflammatory responses in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy.","authors":"Mengfei Ma, Jianxun Guo, Xiaoying Su, Baocai Ma, Xiufen Wang, Mingyu Wangshao, Kai Zhong, Yueying Wang, Guoyu Yang, Yingqian Han","doi":"10.1007/s00011-025-02063-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02063-y","url":null,"abstract":"Objective: This study investigates the role of the aryl hydrocarbon receptor (AhR) in lipopolysaccharide (LPS)-induced inflammatory responses in IPEC-J2 cells.Methods: Inflammatory responses were triggered in IPEC-J2 cells using 5 μg/ml LPS. AhR was activated with tryptophan or FICZ and knocked down via RNA interference. PINK1/Parkin-mediated mitophagy was activated using CCCP and inhibited by PINK1 knockdown. Inflammatory mediators and pathway proteins were analyzed through ELISA, RT-qPCR, western blot, and immunofluorescence. Mitochondrial function was assessed by measuring ROS, ATP, and mitochondrial membrane potential. The interaction between AhR and PINK1 was examined using dual-luciferase reporter assays.Results: The IDO1/AhR signaling axis was activated in LPS-stimulated IPEC-J2 cells. AhR activation was found to attenuate LPS-induced inflammatory responses, whereas AhR knockdown exacerbated these responses. Mechanistic investigations demonstrated that AhR activation alleviated LPS-induced mitochondrial damage. Activating PINK1/Parkin-mediated mitophagy successfully countered the increased inflammatory response in IPEC-J2 cells after AhR knockdown. Moreover, blocking PINK1 reversed the anti-inflammatory effects of FICZ. Dual-luciferase reporter assays revealed that AhR acts as a crucial transcription factor by directly binding to the promoter region, thereby initiating PINK1 transcription.Conclusions: AhR reduces LPS-induced inflammatory response in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy, with AhR directly engaging the PINK1 promoter to enhance its transcription. Targeting AhR may present a novel strategy for the prevention and management of Escherichia coli-induced diarrhea in piglets.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"98"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical outcomes of anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in coronary artery disease patients: a systemic review and meta-analysis of 37,056 individuals from 32 randomized trials. 抗炎疗法抑制冠心病患者NLRP3/IL-1β/IL-6/CRP通路的临床结果：一项来自32项随机试验的37,056人的系统评价和荟萃分析

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02058-9

Yannan Pan, Fangfang Fan, Jie Jiang, Yan Zhang

{"title":"Clinical outcomes of anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in coronary artery disease patients: a systemic review and meta-analysis of 37,056 individuals from 32 randomized trials.","authors":"Yannan Pan, Fangfang Fan, Jie Jiang, Yan Zhang","doi":"10.1007/s00011-025-02058-9","DOIUrl":"10.1007/s00011-025-02058-9","url":null,"abstract":"Background: Treatment effects of anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in coronary artery disease (CAD) had conflicting results. The study aims to evaluate efficacy and safety outcomes of treatments inhibiting this pathway.Methods: Cochrane Library, Embase, Pubmed, and ClinicalTrials.gov were searched for randomized controlled trials evaluating therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in CAD patients. Relative risks (RR) with 95% confidence intervals (CI) were calculated.Results: 32 studies and 37,056 individuals were included. Anti-inflammatory therapies inhibiting the pathway reduced the risks of myocardial infarction (MI) (RR 0.85, 95% CI 0.78-0.93) and coronary revascularization (RR 0.80, 95% CI 0.74-0.86), with no benefits in major adverse cardiovascular events (MACE), heart failure (HF), stroke, cardiovascular or all-cause mortality. Colchicine reduced the risks of MACE, MI, and coronary revascularization. IL-1 inhibitors reduced the risks of coronary revascularization, with potential benefits in MI and HF. Increased risks of infections, gastrointestinal adverse effects, and injection site reactions were found. Meta-regression analysis demonstrated that post-treatment hsCRP/CRP was correlated with MACE (p < 0.001) and MI (p = 0.048) and post-treatment IL-6 was associated with MI (p = 0.033).Conclusion: Anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway had satisfying safety profiles and were beneficial in preventing MI and coronary revascularization in CAD patients despite no benefits in stroke, cardiovascular, or all-cause mortality.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"99"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12206679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of key genes and development of an identifying machine learning model for sepsis. 关键基因的鉴定和败血症识别机器学习模型的开发。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02068-7

Zhonghao Li, Shengsong Chen, Nan Gao, Jie Chen, Ying Qin, Guoqiang Zhang

{"title":"Identification of key genes and development of an identifying machine learning model for sepsis.","authors":"Zhonghao Li, Shengsong Chen, Nan Gao, Jie Chen, Ying Qin, Guoqiang Zhang","doi":"10.1007/s00011-025-02068-7","DOIUrl":"https://doi.org/10.1007/s00011-025-02068-7","url":null,"abstract":"Objective and design: This study aims to identify key genes of sepsis and construct a model for sepsis identification through integrated multi-organ single-cell RNA sequencing (scRNA-seq) and machine learning.Material or subjects: Datasets downloaded from the Gene Expression Omnibus (GSE207363, GSE207651, GSE185263, GSE69063 and GSE134347) were used.Methods: ScRNA-seq data extracted from heart (GSE207363) and lung tissues (GSE207651) of septic mice were processed and analyzed using the Seurat package in R. Key genes were identified as present in both heart and lung tissues, resulting from the overlap of three analyses along with differential expression analyses. We then used support vector machine recursive feature elimination to construct a model for sepsis identification based on these key genes. The GSE185263 dataset was used for training, while GSE69063 and GSE134347 were used for testing. The accuracy of the model in identifying of sepsis was validated by analyzing the area under the receiver operating characteristic curve (AUROC) using the test datasets.Results: Thirteen genes were initially identified as key genes, and after translation to their human homologs, ten genes remained. The optimal SVM-RFE model incorporated eight of these genes (CAMP, CD74, HLA-DQA1, HLA-DQB1, HLA-DMA, HLA-DRB5, and LYZ). In the two test datasets, the AUROC value for the accuracy of the model in identifying of sepsis was 0.904 and 0.924, respectively.Conclusions: We have identified several key genes and developed a machine learning model for sepsis identification. Further studies are needed to validate our findings.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"100"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biological attributes of zinc-dependent endopeptidases in endothelial dysfunction associated with sepsis: a narrative review. 锌依赖性内肽酶在脓毒症相关内皮功能障碍中的生物学特性：一篇叙述性综述。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02056-x

Óscar Gorgojo-Galindo, María Álvarez-Bardón, Adrián García-Concejo, Rocío López-Herrero, María Heredia-Rodríguez, Eduardo Tamayo, Hugo Gonzalo-Benito

引用次数: 0

MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner. MitoQ以柠檬酸合酶依赖的方式减轻脓毒症急性肺损伤中的线粒体损伤。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-24 DOI: 10.1007/s00011-025-02055-y

Jiaojiao Sun, Sihao Jin, Zhiqiang Wang

{"title":"MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner.","authors":"Jiaojiao Sun, Sihao Jin, Zhiqiang Wang","doi":"10.1007/s00011-025-02055-y","DOIUrl":"10.1007/s00011-025-02055-y","url":null,"abstract":"Sepsis is a systemic inflammatory disease caused by severe infection, involving multiple organs in the body, with the lungs being the most susceptible, leading patients to develop acute lung injury (ALI). Mitoquinone Mesylate (MitoQ) is an antioxidant specifically designed to target mitochondria, and it has anti-aging and antioxidant properties. This study aimed to investigate the protective effects of MitoQ on sepsis-induced ALI and its mechanisms. C57BL/6 mice were used to establish the cecal ligation and puncture (CLP) model of sepsis and were orally administered or not administered MitoQ for two weeks. MitoQ effectively alleviated sepsis-induced lung tissue damage, inflammatory responses, oxidative stress, and apoptosis. Furthermore, MitoQ significantly inhibited oxidative stress and mitochondrial damage in pulmonary macrophages. Mechanistically, MitoQ upregulated the mRNA and protein levels of citrate synthase (CS) in lung tissues and pulmonary macrophages. Silencing the CS gene with siRNA significantly reduced the protective effects of MitoQ against oxidative stress, inflammation, and cell apoptosis. In conclusion, MitoQ alleviates sepsis-induced ALI by preserving mitochondrial function.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"92"},"PeriodicalIF":4.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12187896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease. 外泌体作为自身免疫性炎症的免疫调节剂：对原发性Sjögren病的影响。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-13 DOI: 10.1007/s00011-025-02053-0

Yanggang Hong, Siyan Chen, Xiaoyang Jiang, Jinwen Zhang, Xinyue Liang, Jiani Yao, Sheng Gao, Chunyan Hua

{"title":"Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease.","authors":"Yanggang Hong, Siyan Chen, Xiaoyang Jiang, Jinwen Zhang, Xinyue Liang, Jiani Yao, Sheng Gao, Chunyan Hua","doi":"10.1007/s00011-025-02053-0","DOIUrl":"https://doi.org/10.1007/s00011-025-02053-0","url":null,"abstract":"Primary Sjögren's disease (pSD) is a systemic autoimmune disorder characterized by exocrine gland dysfunction and lymphocytic infiltration, leading to dry mouth and eyes. Increasing evidence implicates extracellular vesicles, particularly exosomes, as critical mediators of immune regulation in pSD. This review outlines the biogenesis, molecular composition, and immunomodulatory functions of exosomes, and summarizes their emerging roles in the pathogenesis, diagnosis, and potential treatment of pSD. Exosomes derived from immune and glandular cells carry diverse cargoes, such as miRNAs, proteins, and nucleic acids, that modulate disease-relevant immune pathways. For example, exosomal miR-BART13-3p from Epstein-Barr virus-infected B cells suppresses STIM1 and AQP5, impairing salivary gland function, while PD-L1-enriched exosomes from mesenchymal stem cells inhibit T follicular helper cell polarization via the PI3K/AKT pathway, thereby modulating B-cell activation. Additional exosomal cargoes affect Th17/Treg balance, inflammasome activation, and type I interferon signaling. We also highlight the diagnostic potential of disease-specific exosomal markers in plasma and discuss advances in preclinical studies using exosomes as therapeutic agents. However, significant challenges remain, including cargo heterogeneity, lack of standardized isolation methods, and limited clinical data, all of which hinder the translation of exosome-based therapies into clinical practice. By integrating mechanistic and translational findings, this review provides a comprehensive perspective on the immunological and clinical relevance of exosomes in pSD. These insights may guide future development of diagnostic biomarkers and targeted therapies in autoimmune diseases.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"91"},"PeriodicalIF":4.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0