Inflammation Research最新文献

{"title":"Bilirubin metabolism and its application in disease prevention: mechanisms and research advances.","authors":"Yue Zhang, Haoni Luan, Peng Song","doi":"10.1007/s00011-025-02049-w","DOIUrl":"https://doi.org/10.1007/s00011-025-02049-w","url":null,"abstract":"<p><p>The role of bilirubin, a product of heme metabolism, has evolved from a traditionally perceived metabolic waste product to a critical molecule with diverse biological roles. This article comprehensively reviews the metabolic functions of bilirubin and advances in its application for disease prevention. Bilirubin is primarily derived from hemoglobin catabolism in senescent erythrocytes. It is subsequently metabolized and excreted by the liver through tightly regulated processes involving enzymes, nuclear receptors, hormones, and pharmaceuticals. Bilirubin exhibits diverse physiological functions, including antioxidant, anti-inflammatory, and immunomodulatory activities. Owing to its unique chemical structure, bilirubin scavenges free radicals, inhibits lipid peroxidation, and protects cells across multiple systems. By suppressing the NF-κB signaling pathway, it reduces inflammatory factor release and mitigates chronic inflammation. Additionally, it modulates immune cell activity to maintain homeostasis, offering therapeutic potential for autoimmune and infectious diseases. Bilirubin demonstrates significant potential in disease prevention. In cardiovascular diseases, it attenuates atherosclerosis and mitigates myocardial ischemia/reperfusion injury. For metabolic disorders, it improves insulin resistance, regulates blood glucose, and reduces hepatic steatosis, offering therapeutic benefits for diabetes and non-alcoholic fatty liver disease. In neurological conditions, its antioxidant and anti-inflammatory properties hold promise for preventing and managing neurodegenerative diseases and neonatal bilirubin encephalopathy. Although research on bilirubin has advanced significantly, its intracellular targets and molecular interaction networks remain incompletely understood, and numerous challenges hinder its clinical translation. Future efforts should leverage multi-omics technologies to elucidate its mechanisms, develop intelligent and personalized therapeutics, and conduct large-scale clinical trials to accelerate translational applications and improve patient outcomes.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"81"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142376","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}

{"title":"Lipopolysaccharide induces retention of E-cadherin in the endoplasmic reticulum and promotes hybrid epithelial-to-mesenchymal transition of human embryonic stem cells-derived expandable lung epithelial cells.","authors":"Türkan Portakal, Vítězslav Havlíček, Jarmila Herůdková, Vendula Pelková, Tereza Gruntová, Rıza Can Çakmakci, Hana Kotasová, Aleš Hampl, Petr Vaňhara","doi":"10.1007/s00011-025-02041-4","DOIUrl":"10.1007/s00011-025-02041-4","url":null,"abstract":"<p><strong>Background: </strong>Lipopolysaccharide (LPS)-induced inflammation of lung tissues triggers irreversible alterations in the lung parenchyma, leading to fibrosis and pulmonary dysfunction. While the molecular and cellular responses of immune and connective tissue cells in the lungs are well characterized, the specific epithelial response remains unclear due to the lack of representative cell models. Recently, we introduced human embryonic stem cell-derived expandable lung epithelial (ELEP) cells as a novel model for studying lung injury and regeneration.</p><p><strong>Methods: </strong>ELEPs were derived from the CCTL 14 human embryonic stem cell line through activin A-mediated endoderm specification, followed by further induction toward pulmonary epithelium using FGF2 and EGF. ELEPs exhibit a high proliferation rate and express key structural and molecular markers of alveolar progenitors, such as NKX2-1. The effects of Escherichia coli LPS serotype O55:B5 on the phenotype and molecular signaling of ELEPs were analyzed using viability and migration assays, mRNA and protein levels were determined by qRT-PCR, western blotting, and immunofluorescent microscopy.</p><p><strong>Results: </strong>We demonstrated that purified LPS induces features of a hybrid epithelial-to-mesenchymal transition in pluripotent stem cell-derived ELEPs, triggers the unfolded protein response, and upregulates intracellular β-catenin level through retention of E-cadherin within the endoplasmic reticulum.</p><p><strong>Conclusions: </strong>Human embryonic stem cell-derived ELEPs provide a biologically relevant, non-cancerous lung cell model to investigate molecular responses to inflammatory stimuli and address epithelial plasticity. This approach offers novel insights into the fine molecular processes underlying lung injury and repair.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"82"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142400","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}

{"title":"Targeting carboxypeptidase A/B activity with the phosphinic inhibitor C28 reduces the asthmatic response in a mouse model of house dust mite-induced asthma.","authors":"Venkata Sita Rama Raju Allam, David Montpeyó, Fabrice Beau, Sowsan Taha, Ida Waern, Srinivas Akula, Francesc Xavier Avilés, Julia Lorenzo, Laurent Devel, Gunnar Pejler, Sara Wernersson","doi":"10.1007/s00011-025-02046-z","DOIUrl":"10.1007/s00011-025-02046-z","url":null,"abstract":"<p><strong>Objective: </strong>Metallo-carboxypeptidases are implicated in several pathological contexts but their role in asthma and their potential as therapeutic targets in asthmatic settings are only partly understood. This study sought to investigate whether inhibition of carboxypeptidase activity of A and B-type could mitigate asthma-like symptoms in a mouse model of allergic airway inflammation.</p><p><strong>Methods: </strong>BALB/c mice were sensitized and challenged with repeated intranasal instillations of 10 µg house dust mite extract. Prior to each instillation, groups of mice received intraperitoneally from 0.2 to 1 mg/kg of compound 28, a phosphinic inhibitor of A/B-type carboxypeptidases. Manifestations of asthma-like features were assessed, including airway hyperresponsiveness, airway inflammation, lung histopathology and inflammatory markers.</p><p><strong>Results: </strong>Treatment with compound 28 protected against airway hyperresponsiveness and profoundly reduced the house dust mite-induced inflammation both in airways and in lung tissue. Moreover, compound 28 could mitigate airway smooth muscle and goblet cell remodelling as well as inflammatory gene expression in the lungs.</p><p><strong>Conclusions: </strong>Compound 28 could suppress multiple features of asthma in a physiologically relevant mouse model, reinforcing the potential of targeting A/B type carboxypeptidases for therapeutic purposes in allergic asthma.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"80"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142405","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}

{"title":"Crosstalk between N6-methyladenosine modification and ncRNAs in rheumatic diseases: therapeutic and diagnostic implications.","authors":"Jianting Wen, Jian Liu, Lei Wan, Yue Sun, Fanfan Wang","doi":"10.1007/s00011-025-02034-3","DOIUrl":"https://doi.org/10.1007/s00011-025-02034-3","url":null,"abstract":"<p><strong>Background: </strong>In eukaryotic cells, N6-methyladenosine (m6A) is the most prevalent RNA methylation modification and plays a fundamental role in regulating diverse biological processes through the modulation of non-coding RNA (ncRNA) expression and activity. The role of m6A modification in developing rheumatic diseases is crucial but remains inadequately studied.</p><p><strong>Methods: </strong>Characterized by pain and inflammation, rheumatic diseases like rheumatoid arthritis (RA), osteoarthritis (OA), ankylosing spondylitis (AS), and systemic lupus erythematosus (SLE) are autoimmune disorders. Recent findings emphasize the importance of m6A modifications and non-coding RNAs in the biological processes underlying rheumatic diseases.</p><p><strong>Results: </strong>This review elucidates the fundamental concept of m6A modification and the associated research methodologies. Subsequently, it systematically consolidates modern knowledge on the influence of m6A regulators and m6A modification-related ncRNAs on rheumatic diseases, incorporating perspectives on traditional Chinese medicine interventions.</p><p><strong>Conclusions: </strong>Offering a comprehensive overview of m6A-related ncRNAs in the context of rheumatic diseases, this review proposes new therapeutic avenues by targeting m6A modification pathways.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"79"},"PeriodicalIF":4.8,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119640","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}

{"title":"Paricalcitol promotes the maturation of immune granulomas in an experimental model of superoxide dismutase A-induced inflammation.","authors":"Ablyakimov Et, Kriventsov Ma, Kubyshkin Av, Maxim A Kriventsov","doi":"10.1007/s00011-025-02050-3","DOIUrl":"https://doi.org/10.1007/s00011-025-02050-3","url":null,"abstract":"<p><strong>Background: </strong>- Granulomatous inflammation is a hallmark of several chronic inflammatory diseases, characterized by the formation of immune granulomas. The vitamin D receptor (VDR) and its ligands, such as paricalcitol, have demonstrated immunomodulatory effects on various immune cell subpopulations, including macrophages, dendritic cells, and T-cells. However, the precise role of VDR activation in granuloma formation and the associated immune regulatory pathways, including the PD-1/PD-L1 axis, remains poorly understood. This study aimed to evaluate the effects of paricalcitol, a selective VDR agonist, on granuloma formation and immune cell composition in an experimental model of superoxide dismutase A (SoDA)-induced inflammation, with a focus on antigen-presenting cells (including CD68 + and CD1a + cells), T- and B-cell populations, and PD-L1 expression.</p><p><strong>Materials and methods: </strong>- The study involved 90 male Wistar rats divided into control and experimental groups. Experimental animals received paricalcitol intraperitoneally at different time points relative to sensitization with SoDA and complete Freund's adjuvant. Granulomatous infiltrates were evaluated histologically, and the cellular composition was assessed via immunohistochemistry using markers such as CD68, CD3, CD1a, CD20, and PD-L1. Statistical analysis included quantitative morphometry and group comparisons.</p><p><strong>Results: </strong>- Paricalcitol administration significantly influenced granuloma development, with groups receiving treatment before (E1) or at the time of sensitization (E2) showing a reduction in immature granulomas and an increase in mature granulomas compared to the control groups. Enhanced macrophage differentiation, characterized by increased multinucleated giant cells and epithelioid cells, was observed. Additionally, there was a significant increase in PD-L1 expression in granulomatous infiltrates of treated groups, particularly in peripherally located immune cells. These effects were accompanied by a modulation of T-cell responses, including a reduction in CD3 + T-cell population.</p><p><strong>Conclusion: </strong>- The findings suggest that paricalcitol promotes granuloma stabilization and maturation by modulating VDR-mediated immune pathways, including maturation and transformation of macrophages into epithelioid and giant multinucleated cells, increase in number of CD1a + cells, and PD-1/PD-L1 axis regulation. The ability of paricalcitol to enhance PD-L1 expression through the VDR-mediated pathways provides additional evidence for its role in preventing excessive immune responses and highlights the therapeutic potential of VDR agonists in managing granulomatous inflammation.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"78"},"PeriodicalIF":4.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989738","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}

{"title":"Shared genetic association between inflammatory bowel disease and acute myeloid leukemia: insights from mendelian randomization and transcriptomic analyses.","authors":"Yanqun Zhou, Xiongfeng Zhang, Shangjin Yin, Yuhong Yao, Tao Chen, Liming Huang, Zenghui Liu","doi":"10.1007/s00011-025-02038-z","DOIUrl":"https://doi.org/10.1007/s00011-025-02038-z","url":null,"abstract":"<p><strong>Background: </strong>Observational studies suggest that a history of inflammatory bowel disease (IBD) is associated with the onset of acute myeloid leukemia (AML), often attributed to drug use. However, these findings are inconsistent. This study aimed to assess the causal relationship between IBD and AML, identify shared pathogenesis, and discover diagnostic and prognostic markers and potential therapeutic drugs.</p><p><strong>Methods: </strong>Two-sample Mendelian randomization (MR) was employed to analyze genetic associations between IBD [ulcerative colitis (UC) and Crohn's disease (CD)] and AML. Transcriptomic data from gene expression omnibus (GEO) identified differentially expressed genes (DEGs) in UC, AML, and controls. Weighted Gene Co-expression Network Analysis (WGCNA) and enrichment analyses [Gene Multiple Association Network Integration Algorithm (GeneMANIA), Kyoto Encyclopedia of Genes and Genomes (KEGG), Ractom pathway] and Gene Ontology (GO) explored shared genetic pathways. Receiver Operating Characteristic (ROC) curve and survival analyses screened diagnostic and prognostic markers. Cibersort and GSVA were employed to analyze the proportion of immune cells in UC and AML datasets, as well as to assess the association of specific genes with immune infiltration. The Drug Signatures Database (DSigDB) and Autodock molecular docking identified potential therapeutic small molecules.</p><p><strong>Results: </strong>MR analysis revealed a causal association between UC and the onset of AML. Differential expression and WGCNA analyses identified 23 co-driver genes regulated by Signal Transducer and Activator of Transcription 3 (STAT3) and Activating Transcription Factor 4 (AFT4), enriched in immune, inflammatory, and cell proliferation pathways. Tissue Inhibitor of Metalloproteinases 1 (TIMP1) and F2R-Like Trypsin Receptor 1 (F2RL1) were identified as practical diagnostic and prognostic markers for AML, with high TIMP1 and low F2RL1 expression promoting an immunosuppressive and inflammatory tumor microenvironment. Quercetin was identified as a promising candidate for UC-associated AML.</p><p><strong>Conclusions: </strong>UC is a risk factor for AML pathogenesis. TIMP1 and F2RL1 are diagnostic and prognostic markers for UC-associated AML, potentially facilitating AML development through sustained inflammation and an immunosuppressive tumor microenvironment. Quercetin, a potential TIMP1 and F2RL1 inhibitor, may mitigate UC-AML transformation, providing insights into UC management, AML monitoring, and preventive therapy development.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"77"},"PeriodicalIF":4.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965376","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}

{"title":"The role of fatty acid metabolism on B cells and B cell-related autoimmune diseases.","authors":"Yanmei Gong, Ruiqi Xu, Guohui Gao, Simiao Li, Ying Liu","doi":"10.1007/s00011-025-02042-3","DOIUrl":"https://doi.org/10.1007/s00011-025-02042-3","url":null,"abstract":"<p><p>Fatty acid metabolism plays a critical role in regulating immune cell function, including B cells, which are central to humoral immunity and the pathogenesis of autoimmune diseases. Emerging evidence suggests that fatty acid metabolism influences B cell development, activation, differentiation, and antibody production, thereby impacting B cell-related autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS). In this review, we discuss the mechanisms by which fatty acid metabolism modulates B cell biology, including energy provision, membrane composition, and signaling pathways. We highlight how alterations in fatty acid synthesis, oxidation, and uptake affect B cell function and contribute to autoimmune pathogenesis. Additionally, we explore the therapeutic potential of targeting fatty acid metabolism in B cells to treat autoimmune diseases. Understanding the interplay between fatty acid metabolism and B cell immunity may provide novel insights into the development of precision therapies for B cell-mediated autoimmune disorders.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"75"},"PeriodicalIF":4.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995641","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}

{"title":"COVID-19 mRNA-1273 vaccination induced mast cell activation with strongly elevated Th₂ cytokines in a systemic mastocytosis patient.","authors":"Matthias Weiss-Tessbach, Teresa Haider, Aoife Gowran, Lorenz Schubert, Jakob Mühlbacher, Jelena Brankovic, Markus Wahrmann, Bernd Jilma, Thomas Boehm","doi":"10.1007/s00011-025-02032-5","DOIUrl":"https://doi.org/10.1007/s00011-025-02032-5","url":null,"abstract":"<p><strong>Objective and design: </strong>SARS-CoV-2 vaccines are recommended for mastocytosis patients. We describe clinical symptoms, chemokine, cytokine, metabolomic and lipidomic derangements in a systemic mastocytosis patient following mRNA-1273 booster vaccination.</p><p><strong>Methods: </strong>Twenty-eight chemokines and cytokines, 41 amino acids and 16 lipid classes were quantified with state-of-the-art methods.</p><p><strong>Results: </strong>Mast cell activation (MCA) symptoms started 24 h after the mRNA-1273 booster vaccination with significant metabolic, lipidomic and cytokine derangements. Histamine concentrations peaked at life-threatening 18 ng/ml concomitant with high tryptase. Peak plasma IL-1Ra, IL-5, IL-6, IL-10, IL-11, CXCL10 and GM-CSF concentrations were elevated 54-, 4.9-, 85-, 54-, 6.1-, 19- and 6.4-fold respectively. Tocilizumab, an IL-6 receptor antagonist, was administered 6 h after admission, because of the highly elevated IL-6 concentrations. More than one year later IL-6 was highly elevated during another MCA attack likely caused by a PCR-proven SARS-CoV-2 infection and tocilizumab was again used. Clinical symptoms improved during the following 12 h similar to the vaccine booster MCA attack.</p><p><strong>Conclusions: </strong>A mRNA-1273 first booster vaccination likely caused a delayed severe MCA attack with highly elevated Th₂-biased cytokines with metabolic and lipidomic derangements. Administration of an IL-6 receptor blocker during both MCA attacks might have shortened the duration of clinical symptoms.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"71"},"PeriodicalIF":4.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998870","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}

{"title":"Identification of ferroptosis-related genes and potential drugs in osteoarthritis.","authors":"Chao Song, Baoxin Shen, Chaoqi Chen, Lei Yang, Chi Zhang, Fei Liu, Feng Chen, Xiaofei Wu","doi":"10.1007/s00011-025-02040-5","DOIUrl":"https://doi.org/10.1007/s00011-025-02040-5","url":null,"abstract":"<p><strong>Background: </strong>Osteoarthritis (OA) is a common chronic degenerative joint disease in orthopedics, and ferroptosis is a newly identified mode of cell death present in OA. Inhibition of inflammatory cytokine expression and modulation of chondrocyte ferroptosis related pathways may be novel strategies for the treatment of OA. The purpose of this work was to uncover prospective biomarkers and molecular processes of ferroptosis in OA, as well as to better understand the molecular mechanisms of ferroptosis in OA treated with resveratrol.</p><p><strong>Material and methods: </strong>We obtained OA gene expression profiles from the Gene Expression Omnibus (GEO) database. OA-expressed ferroptosis-related genes were identified using Genecards data, differential gene analysis, and weighted gene co-expression network analysis. Enrichment analysis was utilized to identify signaling pathways and molecular mechanisms linked with ferroptosis in OA, while immune infiltration analysis indicated immune cell infiltration in OA. The action targets of resveratrol were taken from the TCM database to determine the therapeutic targets of resveratrol for the treatment of OA. To validate the molecular process, molecular docking was performed using the therapeutic targets' enrichment analysis. Finally, in vitro investigations confirmed the molecular mechanism of ferroptosis in resveratrol-treated OA.</p><p><strong>Results: </strong>Bioinformatic analysis identified 462 OA ferroptosis gene sets, with GPX4, TFRC, SLC7A11, EGFR, and IL1B serving as significant hub genes. Enrichment analysis revealed that ferroptosis was also linked to animal mitophagy, the FoxO signaling pathway, the Toll-like receptor signaling pathway, the PI3K-Akt signaling pathway, inflammation, immune response activation, and cellular autophagy. The immune infiltration data revealed that T_cells_CD4_memory_resting, T_cells_CD4_memory_activated, NK_cells_activated, and Mast_cells_activated were considerably infiltrated in OA. Resveratrol ameliorated OA via modulating autophagy and ferroptosis via GPX4, TFRC, SLC7A11, EGFR, and IL1B, according to a mechanistic study.</p><p><strong>Conclusion: </strong>We discovered the mechanism of GPX4, TFRC, SLC7A11, and EGFR, IL1B ferroptosis-related genes in OA, and preliminary evidence suggests that resveratrol improves OA by regulating ferroptosis and immunological processes, which may give a new route for OA treatment.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"70"},"PeriodicalIF":4.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014870","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}

{"title":"Advances in anti-inflammatory treatment of sepsis-associated acute respiratory distress syndrome.","authors":"Nana Zhang, Hewei Zhang, Li Yu, Qiang Fu","doi":"10.1007/s00011-025-02043-2","DOIUrl":"https://doi.org/10.1007/s00011-025-02043-2","url":null,"abstract":"<p><p>Sepsis is characterized by a dysregulated host response to infection, leading to organ dysfunction and associated with significant morbidity and mortality, posing a critical challenge to global public health. Among its complications, sepsis frequently causes acute respiratory distress syndrome (ARDS), which has a high incidence and mortality rate, particularly in intensive care units (ICUs). Currently, the management of sepsis-induced ARDS is largely limited to supportive care, as no specific pharmacological treatments are available. The progression of sepsis to ARDS is driven by severe inflammation and cytokine storms, highlighting the importance of anti-inflammatory therapies as a primary treatment focus. We summarize conventional drugs and emerging treatments targeting excessive inflammatory responses in sepsis-associated ARDS, reviewing progress in basic research and clinical trials. Additionally, we discuss current research challenges to propose future directions for anti-inflammatory treatments, aiming to develop highly effective drugs with better clinical translation potential.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"74"},"PeriodicalIF":4.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008594","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}