Inflammation Research最新文献_第4页

Mechanistic and therapeutic insights into the function of N6-methyladenosine in arthritic diseases. n6 -甲基腺苷在关节炎疾病中的作用机制和治疗见解。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-01-07 DOI: 10.1007/s00011-024-01969-3

Xinyue Zhou, Yajie Wu, Yingqiu Song, Bing Wang, Yikang Cai, Chenggui Miao

{"title":"Mechanistic and therapeutic insights into the function of N6-methyladenosine in arthritic diseases.","authors":"Xinyue Zhou, Yajie Wu, Yingqiu Song, Bing Wang, Yikang Cai, Chenggui Miao","doi":"10.1007/s00011-024-01969-3","DOIUrl":"https://doi.org/10.1007/s00011-024-01969-3","url":null,"abstract":"Objective: Arthritis is a class of diseases, characterized by joint and surrounding inflammation, accompanied by joint swelling, pain, dysfunction. According to different factors, arthritis can be divided into osteoarthritis, rheumatoid arthritis, ankylosing spondylitis and so on. N6-methyladenosine (m6A) is the most common internal modification of eukaryotic mRNA and is involved in splicing, stabilization, output and degradation of RNA metabolism. This review systematically summarized current insights into the mechanism of m6A in arthritis.Methods: The studies related to the involvement of m6A in the pathogenesis of arthritis reported in PubMed, Google scholar, and other open source literatures were investigated to evaluate the important roles of m6A in arhtritis, and the clinical relevances.Results and conclusions: M6A methylation regulators play the roles of writers, erasers, and readers, are crucial for regulating gene expression, and play important roles in many biological processes such as virus replication and cell differentiation. In addition, more and more studies have shown that m6A is closely related to the development of arthritis. As a new therapeutic target for arthritis, m6A has a wide influence on the pathological mechanism of arthritis. However, further research is needed to determine how m6A affects arthritis pathology and its use in target therapy and diagnosis.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"7"},"PeriodicalIF":4.8,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947998","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

Targeting mitochondrial function as a potential therapeutic approach for allergic asthma. 靶向线粒体功能作为过敏性哮喘的潜在治疗方法。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-01-07 DOI: 10.1007/s00011-024-01972-8

Daichi Chen, Wanhua Wu, Jianing Li, Xueqin Huang, Su Chen, TingTing Zheng, Gonghua Huang, Suidong Ouyang

引用次数: 0

Causal genes identification of giant cell arteritis in CD4+ Memory t cells: an integration of multi-omics and expression quantitative trait locus analysis. CD4+记忆t细胞巨细胞动脉炎的致病基因鉴定：多组学和表达数量性状位点分析的结合

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-01-07 DOI: 10.1007/s00011-024-01965-7

Qiyi Yu, Yifan Wu, Xianda Ma, Yidong Zhang

{"title":"Causal genes identification of giant cell arteritis in CD4+ Memory t cells: an integration of multi-omics and expression quantitative trait locus analysis.","authors":"Qiyi Yu, Yifan Wu, Xianda Ma, Yidong Zhang","doi":"10.1007/s00011-024-01965-7","DOIUrl":"https://doi.org/10.1007/s00011-024-01965-7","url":null,"abstract":"Background: Giant cell arteritis (GCA) is a prevalent artery and is strongly correlated with age. The role of CD4+ Memory T cells in giant cell arteritis has not been elucidated.Method: Through single-cell analysis, we focused on the CD4+ Memory T cells in giant cell arteritis. eQTL analysis and mendelian randomization analysis identified the significant genes which have a causal effect on giant cell arteritis risk. CD4+ Memory T cells were subsequently divided into gene-positive and gene-negative groups, then further single-cell analysis was conducted. Mendelian randomization of plasma proteins, blood-urine biomarkers and metabolites were also performed. Eventually, the PMA induced Jurkat cell lines were used for biological experiments to explore the specific functions of significant causal genes in CD4+ Memory T cells.Results: Similarity of CD4+ Memory T cells in GCA and old samples were explored. DDIT4 and ARHGAP15 were identified as significant risk genes via mendelian randomization. The CD4+ Memory T cells were then divided into DDIT4 ± or ARHGAP15 ± groups, and further single-cell analysis indicated the differences in aspects involving intercellular communication, functional pathways, protein activity, metabolism and drug sensitivity between positive and negative groups. In vitro experiments, including overexpression and knockdown, demonstrated that DDIT4 leading to a chronic, low-intensity inflammatory state in CD4+ Memory T cells, eventually promoting the development of GCA.Conclusion: DDIT4 and ARHGAP15 have significant causal effects on giant cell arteritis risk. Specifically, DDIT4 exhibit pro-inflammatory effects on GCA via promotes chronic, low-intensity inflammatory in CD4+ Memory T cell.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"3"},"PeriodicalIF":4.8,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946867","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

A universal gene expression signature-based strategy for the high-throughput discovery of anti-inflammatory drugs. 基于通用基因表达特征的抗炎药物高通量发现策略。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-01-07 DOI: 10.1007/s00011-024-01968-4

Juan Feng, Honglei Dang, Xiaoling Zhang, Wenting Huang, Chengmei Ma, Aixiang Zhang, Mimi Hao, Lan Xie

{"title":"A universal gene expression signature-based strategy for the high-throughput discovery of anti-inflammatory drugs.","authors":"Juan Feng, Honglei Dang, Xiaoling Zhang, Wenting Huang, Chengmei Ma, Aixiang Zhang, Mimi Hao, Lan Xie","doi":"10.1007/s00011-024-01968-4","DOIUrl":"https://doi.org/10.1007/s00011-024-01968-4","url":null,"abstract":"Background: Traditional Chinese medicine (TCM) is a valuable resource for drug discovery and has demonstrated excellent efficacy in treating inflammatory diseases. This study aimed to develop a universal gene signature-based strategy for high-throughput discovery of anti-inflammatory drugs, especially Traditional Chinese medicine (TCM).Methods: The disease gene signature of liposaccharide-stimulated THP-1 cells and drug gene signatures of 655 drug candidates were established via sequencing. Anti-inflammatory drugs were screened based on similarities between drug gene signatures and the reversed disease gene signature.Results: Through screening, 83 potential anti-inflammatory drugs were identified. The efficacy of the TCM formula Biyun Powder, along with individual TCMs, Centipedea Herba, Kaempferiae Rhizoma, and Schizonepetae Spica Carbonisata, was verified in vitro or in vivo. Mechanistically, they exerted anti-inflammatory effects by inhibiting the nuclear factor-kappa B pathway. Kaempferol and luteolin were identified as bioactive IκB kinase-β inhibitors in Kaempferiae Rhizoma and Schizonepetae Spica Carbonisata, respectively.Conclusion: We developed a universal gene signature-based approach for the high-throughput discovery of anti-inflammatory drugs that is applicable to compounds and to TCM herbs/formulae and established a workflow (screening, validation of efficacy, and identification of the mechanism of action and bioactive compounds) that can serve as a research template for high-throughput drug research.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"2"},"PeriodicalIF":4.8,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948237","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

MAIT cells modulating the oral lichen planus immune microenvironment: a cellular crosstalk perspective. MAIT细胞调节口腔扁平苔藓免疫微环境：细胞串扰的视角。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-01-07 DOI: 10.1007/s00011-024-01990-6

Qian Mi, Xiaoli Wu, Yuhe Chen, Wenxia Meng

{"title":"MAIT cells modulating the oral lichen planus immune microenvironment: a cellular crosstalk perspective.","authors":"Qian Mi, Xiaoli Wu, Yuhe Chen, Wenxia Meng","doi":"10.1007/s00011-024-01990-6","DOIUrl":"https://doi.org/10.1007/s00011-024-01990-6","url":null,"abstract":"Mucosal-associated invariant T (MAIT) cells, a type of T lymphocytes with innate-like characteristics, are crucial in bridging innate and adaptive immunity. When activated, MAIT cells release various inflammatory molecules and swiftly respond to antigens. Notably, numerous studies highlight the significant impact of MAIT cells on tumors and various immune disorders by influencing the immune microenvironment. Oral lichen planus (OLP) is an immune-mediated inflammatory condition mainly involving T lymphocytes. Previous research primarily focused on T cells alone, neglecting the broader immune environment. However, there is a current growing recognition of the complex interactions among multiple immune cells and inflammatory factors in patients with OLP. This immune microenvironment comprises T lymphocytes, fibroblasts, keratinocytes, dendritic cells, macrophages, inflammation-related cytokines, and chemokines, orchestrating intricate interactions that contribute to OLP initiation and persistence. Therefore, this review consolidates current research on the interplay between MAIT cells and other immune cells within the OLP microenvironment. We also delve into potential mechanisms through which MAIT cells regulate inflammation in patients with OLP, aiming to further explore the role of MAIT cells in these patients.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"10"},"PeriodicalIF":4.8,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947931","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

Editorial expression of concern: Monocytes and lymphocytes as active participants in the pathogenesis of experimental shock. 社论表达的关切：单核细胞和淋巴细胞是实验性休克发病机制的积极参与者。

IF 4.8 3区医学

Inflammation Research Pub Date : 2024-12-01 DOI: 10.1007/s00011-024-01930-4

D Altavilla, F Squadrito, L Ammendolia, G Squadrito, G M Campo, P Canale, M Ioculano, C Musolino, A Alonci, A Sardella, G Urna, A Saitta, A P Caputi

引用次数: 0

Single-cell transcriptome analysis of the mouse lungs during the injury and recovery periods after lipopolysaccharide administration. 单细胞转录组分析小鼠肺部在服用脂多糖后的损伤期和恢复期的情况。

IF 4.8 3区医学

Inflammation Research Pub Date : 2024-12-01 Epub Date: 2024-10-08 DOI: 10.1007/s00011-024-01951-z

Hou-Ping Wang, Jian He, Jian-Rong He, Dan-Dan Li, He Huang, Bing Chen

{"title":"Single-cell transcriptome analysis of the mouse lungs during the injury and recovery periods after lipopolysaccharide administration.","authors":"Hou-Ping Wang, Jian He, Jian-Rong He, Dan-Dan Li, He Huang, Bing Chen","doi":"10.1007/s00011-024-01951-z","DOIUrl":"10.1007/s00011-024-01951-z","url":null,"abstract":"Objective: This study sought to investigate the cellular and molecular alterations during the injury and recovery periods of ALI and develop effective treatments for ALI.Methods: Pulmonary histology at 1, 3, 6, and 9 days after lipopolysaccharide administration mice were assessed. An unbiased single-cell RNA sequencing was performed in alveoli tissues from injury (day 3) and recovery (day 6) mice after lipopolysaccharide administration. The roles of Fpr2 and Dpp4 in ALI were assessed.Results: The most severe lung injury occurred on day 3, followed by recovery entirely on day 9 after lipopolysaccharide administration. The numbers of Il1a+ neutrophils, monocytes/macrophages, and Cd4+ and Cd8+ T cells significantly increased at day 3 after LPS administration; subsequently, the number of Il1a+ neutrophils greatly decreased, the numbers of monocytes/macrophages and Cd4+ and Cd8+ T cells continuously increased, and the number of resident alveolar macrophages significantly increased at day 6. The interactions between monocytes/macrophages and pneumocytes during the injury period were enhanced by the Cxcl10/Dpp4 pair, and inhibiting Dpp4 improved ALI significantly, while inhibiting Fpr2 did not.Conclusions: Our results offer valuable insights into the cellular and molecular mechanisms underlying its progression and identify Dpp4 as an effective therapeutic target for ALI.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2087-2107"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390244","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

Retraction Note: The role of nitric oxide during healing of trauma to the skeletal muscle. 撤稿说明：一氧化氮在骨骼肌创伤愈合过程中的作用。

IF 4.8 3区医学

Inflammation Research Pub Date : 2024-12-01 DOI: 10.1007/s00011-024-01963-9

Lidiane Isabel Filippin, María José Cuevas, Elena Lima, Norma Possa Marroni, Javier Gonzalez Gallego, Ricardo Machado Xavier

引用次数: 0

Molecular mechanism of mechanical pressure induced changes in the microenvironment of intervertebral disc degeneration. 机械压力诱导椎间盘退变微环境变化的分子机制。

IF 4.8 3区医学

Inflammation Research Pub Date : 2024-12-01 Epub Date: 2024-10-08 DOI: 10.1007/s00011-024-01954-w

Fei Liu, Song Chao, Lei Yang, Chaoqi Chen, Wutao Huang, Feng Chen, Zhiwei Xu

{"title":"Molecular mechanism of mechanical pressure induced changes in the microenvironment of intervertebral disc degeneration.","authors":"Fei Liu, Song Chao, Lei Yang, Chaoqi Chen, Wutao Huang, Feng Chen, Zhiwei Xu","doi":"10.1007/s00011-024-01954-w","DOIUrl":"10.1007/s00011-024-01954-w","url":null,"abstract":"Background: Lower back pain, as a typical clinical symptom of spinal degenerative diseases, is emerging as a major social problem. According to recent researches, the primary cause of this problem is intervertebral disc degeneration (IVDD). IVDD is closely associated with factors such as age, genetics, mechanical stimulation (MS), and inadequate nutrition. In recent years, an increasing number of studies have further elucidated the relationship between MS and IVDD. However, the exact molecular mechanisms by which MS induces IVDD remain unclear, highlighting the need for in-depth exploration and study of the relationship between MS and IVDD.Methods: Search for relevant literature on IVDD and MS published from January 1, 2010, to the present in the PubMed database.Results: One of the main causes of IVDD is MS, and loading modalities have an impact on the creation of matrix metalloproteinase, the metabolism of the cellular matrix, and other biochemical processes in the intervertebral disc. Nucleus pulposus cell death induced by MS, cartilage end-plate destruction accompanied by pyroptosis, apoptosis, iron death, senescence, autophagy, oxidative stress, inflammatory response, and ECM degradation interact with one another to form a cooperative signaling network.Conclusion: This review discusses the molecular mechanisms of the changes in the microenvironment of intervertebral discs caused by mechanical pressure, explores the interaction between mechanical pressure and IVDD, and provides new insights and approaches for the clinical prevention and treatment of IVDD.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2153-2164"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390243","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

Macrophage activation syndrome in Sepsis: from pathogenesis to clinical management. 败血症中的巨噬细胞活化综合征：从发病机制到临床管理。

IF 4.8 3区医学

Inflammation Research Pub Date : 2024-12-01 Epub Date: 2024-10-15 DOI: 10.1007/s00011-024-01957-7

Shunyao Chen, Cong Zhang, Jialiu Luo, Zhiqiang Lin, Teding Chang, Liming Dong, Deng Chen, Zhao-Hui Tang

{"title":"Macrophage activation syndrome in Sepsis: from pathogenesis to clinical management.","authors":"Shunyao Chen, Cong Zhang, Jialiu Luo, Zhiqiang Lin, Teding Chang, Liming Dong, Deng Chen, Zhao-Hui Tang","doi":"10.1007/s00011-024-01957-7","DOIUrl":"10.1007/s00011-024-01957-7","url":null,"abstract":"Background: Sepsis represents a significant global health and hygiene challenge. Excessive activation of macrophages in sepsis can result in certain patients displaying characteristics akin to those observed in Macrophage Activation Syndrome (MAS). MAS represents a grave immune system disorder characterized by persistent and severe inflammation within the body. In the context of sepsis, MAS presents atypically, leading some researchers to refer to it as Macrophage Activation-Like Syndrome (MALS). However, there are currently no effective treatment measures for this situation. The purpose of this article is to explore potential treatment methods for sepsis-associated MALS.Objective: The objective of this review is to synthesize the specific pathophysiological mechanisms and treatment strategies of MAS to investigate potential therapeutic approaches for sepsis-associated MALS.Method: We searched major databases (including PubMed, Web of Science, and Google Scholar etc.) for literature encompassing macrophage activation syndrome and sepsis up to Mar 2024 and combined with studies found in the reference lists of the included studies.Conclusion: We have synthesized the underlying pathophysiological mechanism of MALS in sepsis, and then summarized the diagnostic criteria and the effects of various treatment modalities utilized in patients with MAS or MALS. In both scenarios, heterogeneous treatment responses resulting from identical treatment approaches were observed. The determination of whether the patient is genuinely experiencing MALS significantly impacts the ultimate outcomes of therapeutic efficacy. In order to tackle this concern, additional clinical trials and research endeavors are imperative.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2179-2197"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464296","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