Inflammation Research最新文献

{"title":"The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome.","authors":"Abbas Shahi, Zahra Firoozi, Ghaidaa Raheem Lateef Al-Awsi, Ebrahim Mirzaei, Hojjat Shahbazi, Zahra Rezaee, Elham Mohammadisoleimani, Yaser Mansoori, Ali Moravej","doi":"10.1007/s00011-025-02052-1","DOIUrl":"https://doi.org/10.1007/s00011-025-02052-1","url":null,"abstract":"<p><p>The brain's process of creating neural networks that affect functionality or performance is referred to as neurodevelopment. A person's capacity to learn and remember, pay attention, regulate their emotions, socialize, exercise and self-control are just a few of the cognitive and motor abilities that can be affected by abnormal brain development. Numerous neurodevelopmental diseases have been functionally related to abnormalities in innate immune signaling networks. Innate immunity is in charge of the defense of humans against pathogens and tissue damage by triggering inflammation, mainly through sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Some of these inflammatory processes have been shown to be mediated by large multiprotein complexes called inflammasomes which are present in cytosol and play important roles in the immune system. Due to its role in defense against infectious agents, bacteria, viruses, and fungi, NLRP3 is almost the most studied and well-known member of inflammasomes. The involvement of NLRP3 in inflammatory illnesses is evident due to the wide range of triggers and its intricate signaling pathways. In disorders with neurodevelopmental underpinnings, such as autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), schizophrenia (SCZ), obsessive compulsive disorder (OCD), bipolar disorder (BD), Tourette syndrome (TS), etc., neuroinflammation plays a significant role in their pathophysiology. For these reasons, we reviewed the roles of NLRP3 in various neurodevelopmental disorders below.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"90"},"PeriodicalIF":4.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208452","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":"Successful treatment of refractory erythrodermic pemphigus foliaceus with low-dose rituximab and intravenous immunoglobulin.","authors":"Jiawen Zhang, Chengfeng Zhang, Zhongyi Xu, Jun Liang, Qinyuan Zhu","doi":"10.1007/s00011-025-02059-8","DOIUrl":"https://doi.org/10.1007/s00011-025-02059-8","url":null,"abstract":"<p><strong>Background: </strong>Erythrodermic pemphigus foliaceus (EPF) is a severe, often refractory autoimmune disease.</p><p><strong>Method: </strong>We report successful treatment of refractory EPF in a 59-year-old male using low-dose rituximab (RTX) and intravenous immunoglobulin (IVIG).</p><p><strong>Results: </strong>Initial high-dose corticosteroids and IVIG failed, complicated by infections. A modified regimen of RTX (0.5 g) and IVIG (0.4 g/kg/day for three days) every two weeks for two cycles induced remission, with a mild relapse at six months successfully retreated. No infections occurred during 15-month follow-up.</p><p><strong>Conclusion: </strong>This combined therapy using low-dose RTX and IVIG may be a safe and effective option for refractory EPF, potentially minimizing infection risk associated with standard RTX dosing. Further studies are warranted.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"89"},"PeriodicalIF":4.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208451","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":"OptiStack classifier: optimized stacking framework with ensemble feature engineering for enhanced cardiovascular risk prediction.","authors":"M Dhilsath Fathima, S P Raja, K Jayanthi, R Hariharan","doi":"10.1007/s00011-025-02039-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02039-y","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular diseases (CVD) are a leading cause of morbidity and mortality globally, highlighting the urgent need for accurate risk prediction to improve early intervention and management. Traditional models have difficulty capturing the complex interactions between risk factors, which limits their predictive power.</p><p><strong>Objective: </strong>This paper proposes the OptiStack Classifier, an optimized stacking framework developed to enhance CVD risk prediction through ensemble feature engineering and machine learning techniques.</p><p><strong>Methods: </strong>The model uses dimensionality reduction and ensemble feature engineering methods, including polynomial expansion, binning and domain-specific feature transformation, to improve data representation. Principal Component Analysis (PCA) is used to dimensionality reduction, improving computational efficiency. A stacking framework integrates multiple machine learning algorithms as base learners, with Logistic Regression acting as the meta-classifier. Bayesian Optimization is applied for hyperparameter tuning, further boosting predictive performance.</p><p><strong>Results: </strong>The proposed model shows significant improvements in predicting CVD risk, helping with early diagnosis and prevention, which can lead to better health outcomes for patients.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"88"},"PeriodicalIF":4.8,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191732","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":"Interleukin-37 modulates microglial phenotype and inhibits inflammatory response via the MyD88/NF-κB pathway in lipopolysaccharide-induced neuroinflammation.","authors":"Jingwen Zhang, Muhammad Abid Hayat, Yu Si, Tao Guo, Yinying Ni, Qian Wang, Yancheng Hong, Yudie Cao, Sijia He, Zijuan Weng, Fengmei Li, Hao Zuo, Xin Sun, Bo Chen, Jiabo Hu","doi":"10.1007/s00011-025-02048-x","DOIUrl":"https://doi.org/10.1007/s00011-025-02048-x","url":null,"abstract":"<p><strong>Objective: </strong>Interleukin-37 (IL-37), an anti-inflammatory cytokine within the interleukin-1 (IL-1) family, exhibits immunomodulatory properties. Here we evaluate the effects of IL-37 on microglia in neuroinflammation and its potential mechanisms.</p><p><strong>Methods: </strong>C57BL/6 mice were injected intraperitoneally with 1 µg of recombinant human IL-37 protein (rhIL-37), and 24 h later with lipopolysaccharide (LPS) (5 mg/kg) to induce neuroinflammation. After 2-h pretreatment of BV2 cells with rhIL-37 (100 ng/mL), an in vitro model was established by treating with LPS (100 ng/mL). Mice were assessed for behavioral tests, and neuronal damage was evaluated by Nissl staining and hematoxylin and eosin staining. The expression of Iba1, CD86, CD206, and NF-κB were detected by immunofluorescence staining, and inflammatory mediators and pathway proteins were evaluated by ELISA, qRT-PCR, and Western blot.</p><p><strong>Results: </strong>IL-37 significantly ameliorated LPS-induced behavioral deficits and protected mice from inflammatory injury. In vitro experiments suggested that IL-37 modulates polarization of microglia from M1 to M2 phenotype, along with reducing pro-inflammatory cytokine production. Moreover, IL-37 attenuated the production of NF-κB and MyD88.</p><p><strong>Conclusions: </strong>IL-37 regulates microglia against neuroinflammatory responses by blocking the MyD88/NF-κB pathway and shows for the first time how IL-37 influences the phenotype of microglia, suggesting a potential therapeutic target for neuroinflammation.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"87"},"PeriodicalIF":4.8,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173613","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":"Aldosterone induces renal lymphangiogenesis through macrophage-lymphatic endothelial cell transformation and Inhibition by esaxerenone.","authors":"Haixia Guo, Ziqian Liu, Ruyan Lv, Boya Zhang, Panpan Qiang, Xuan Wang, Yi Chang, Fan Yang, Tatsuo Shimosawa, Qingyou Xu, Yunzhao Xiong","doi":"10.1007/s00011-025-02044-1","DOIUrl":"https://doi.org/10.1007/s00011-025-02044-1","url":null,"abstract":"<p><strong>Objective and design: </strong>Inflammation plays a crucial role in the occurrence and development of renal fibrosis. Lymphatic vessels have emerged as new hotspots in the domain of inflammation. Recent studies have revealed that macrophages are involved in lymphangiogenesis through direct and indirect mechanisms. However, the underlying mechanisms of macrophage transdifferentiation into lymphatic endothelial cells (LECs) are still poorly understood.</p><p><strong>Methods: </strong>In vivo, thirty male Wistar rats were randomly divided into a sham group, an aldosterone group and an aldosterone + esaxerenone group. In vitro, Raw 264.7 cells and bone marrow-derived macrophages (BMDMs) were used. H&E, Masson, western blotting, immunohistochemistry, immunofluorescence, flow cytometry, and BMDM tube formation assays were used to assess renal fibrosis and lymphangiogenesis in a rat model of aldosterone-induced renal injury.</p><p><strong>Results: </strong>In this study, we observed pathological renal fibrosis and lymphangiogenesis in 12-week-old rats after aldosterone infusion. In addition, the treatment of rats with esaxerenone, a mineralocorticoid receptor blocker (MRB), significantly reduced renal lymphangiogenesis and fibrosis. Interestingly, we found that aldosterone can activate MR to stimulate macrophages to secrete vascular endothelial growth factor C (VEGF-C) and promote lymphatic angiogenesis.</p><p><strong>Conclusions: </strong>Our data suggest that renal fibrosis occurs in aldosterone-treated rats and that inflammation-induced macrophage transdifferentiation into LECs occurs during this process and that MRB attenuates renal fibrosis and lymphangiogenesis due to inflammatory injury.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"85"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142374","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":"Melatonin inhibits salivary gland epithelial cell ferroptosis via the NRF2/HO-1/GPX4 signaling pathway in primary Sjögren's syndrome.","authors":"Xiuhong Weng, Simin Wang, Qing Wang, Mingbo Wei, Bo Cheng","doi":"10.1007/s00011-025-02047-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02047-y","url":null,"abstract":"<p><strong>Background: </strong>Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by xerostomia and autoimmune sialadenitis. Interferon-γ (IFN-γ) induces ferroptosis in salivary gland epithelial cells (SGECs), leading to salivary gland (SG) hypofunction. We previously demonstrated the beneficial effects of melatonin (MLT) in alleviating SG dysfunction and inflammation in a pSS animal model. However, the precise underlying mechanism remains unclear.</p><p><strong>Methods: </strong>Female NOD/ltj and ICR mice were used as the pSS mouse model and control group, respectively. MLT was administered via intraperitoneal injection to NOD/ltj mice to detect its effect on ferroptosis in SGs. Primary human SGECs and A253 cells were treated with IFN-γand ferroptosis inducers, with or without MLT.</p><p><strong>Results: </strong>Exogenous MLT alleviated pathological SG alterations and promoted saliva production through inhibiting SGEC ferroptosis. MLT inhibited SGEC ferroptosis induced by IFN-γ and ferroptosis inducers via nuclear factor erythroid 2-related factor 2/heme oxygenase-1/glutathione peroxidase 4 (NRF2/HO-1/GPX4) pathway activation. Moreover, MLT suppressed the nuclear factor-kappa B (NF-κB) pathway, which is triggered by ferroptosis in SGECs. Nevertheless, ML385-mediated NRF2 inhibition abrogated the antiferroptotic protective effects of MLT on SGECs.</p><p><strong>Conclusions: </strong>MLT inhibits SGEC ferroptosis through NRF2/HO-1/GPX4 pathway activation and thus attenuates ferroptosis-triggered NF-κB activity. Melatonin represents a potential therapeutic approach for pSS owing to its capacity to regulate ferroptosis.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"84"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142403","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":"Influence of homocysteine on regulating immunothrombosis: mechanisms and therapeutic potential in management of infections.","authors":"Aswathy S Nair, Lloyd Tauro, Harshit B Joshi, Arnab Makhal, Teddy Sobczak, Julien Goret, Antoine Dewitte, Srinivas Kaveri, Harinath Chakrapani, Maria Mamani Matsuda, Manjunath B Joshi","doi":"10.1007/s00011-025-02045-0","DOIUrl":"10.1007/s00011-025-02045-0","url":null,"abstract":"<p><p>Mechanisms controlling innate immune responses and coagulation are interdependent, evolutionarily entangled and make a complex network to form immuno-thrombosis axis which is an integral part of host-defence response. During infections, immunothrombosis generates intravascular scaffold enabling recognition, trap and destruction of pathogens facilitating tissue integrity. However, the accompanying dysregulation fosters into pathologies associated with thrombosis and regulates severity, morbidity and mortality in infections. Several extrinsic and intrinsic factors such as (epi)genetic mechanisms, age, metabolism and lifestyle regulate immunothrombosis during infections. Mounting evidence demonstrates that homocysteine, a metabolic intermediate of methionine synthesis pathway activate cells participating in immuno-thrombosis such as neutrophils, platelets, monocytes and endothelial cells. Interestingly, multiple infections are significantly associated with perturbed homocysteine metabolism. In the present review, we describe mechanistic insights into how homocysteine drives immuno-thrombotic crosstalk that generate a vicious cycle of inflammation and coagulation that fuels organ failure during infections with an emphasis on sepsis, COVID-19, and other infectious diseases caused by parasites, viral, and bacterial pathogens. Subsequently, we discuss therapeutic strategies targeting homocysteine metabolism that may improve clinical outcomes in infections.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"86"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142378","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":"Lung contusion drives lung injury by modifying miRNA cargo in alveolar small extracellular vesicles.","authors":"Keita Nakatsutsumi, Dong Jun Park, Wooil Choi, William Johnston, Katie Pool, Jenny Kezios, Raul Coimbra, Brian P Eliceiri, Todd W Costantini","doi":"10.1007/s00011-025-02051-2","DOIUrl":"10.1007/s00011-025-02051-2","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the micro-RNA (miRNA) cargo of alveolar small extracellular vesicles (sEVs) after lung contusion (LC), which can contribute to the development of trauma-related acute lung injury (ALI).</p><p><strong>Methods: </strong>A mouse model of LC was conducted with a controlled cortical impact device. Bronchoalveolar lavage fluid (BAL) was collected 24 h post-injury and sEVs were purified using size exclusion chromatography. sEVs characteristics and miRNA cargo were analyzed with vesicle flow cytometry and sequencing. Macrophages were treated with BAL sEVs in vitro to assess their pro-inflammatory effect.</p><p><strong>Results: </strong>LC increased lung permeability and caused ALI histologically. LC increased the number of sEVs in the BAL and altered their miRNA cargo. BAL sEVs collected after LC increased pro-inflammatory cytokine release from macrophages.</p><p><strong>Conclusion: </strong>LC increased the mobilization of sEVs to the alveolar space and modified their miRNA cargo that might contribute to the development of ALI by activating the immune response in macrophages.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"83"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142402","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":"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}