Inflammation最新文献

Nrf2 Protects Against Lipoteichoic Acid-Induced Acute Lung Injury By Suppressing SLC24A2-Mediated Ferroptosis. Nrf2通过抑制slc24a2介导的铁凋亡来保护脂质胆酸诱导的急性肺损伤。

IF 5 2区医学

Inflammation Pub Date : 2026-05-09 DOI: 10.1007/s10753-026-02499-2

Ri-Xiang Huang, Tao Lu, Nan-Nan Liu, Jiao-Jiao Sun, Jun Zhu, Min Chen, Dan Chen, Ya-Xian Wu, Yuan Weng, Zhi-Qiang Wang

{"title":"Nrf2 Protects Against Lipoteichoic Acid-Induced Acute Lung Injury By Suppressing SLC24A2-Mediated Ferroptosis.","authors":"Ri-Xiang Huang, Tao Lu, Nan-Nan Liu, Jiao-Jiao Sun, Jun Zhu, Min Chen, Dan Chen, Ya-Xian Wu, Yuan Weng, Zhi-Qiang Wang","doi":"10.1007/s10753-026-02499-2","DOIUrl":"https://doi.org/10.1007/s10753-026-02499-2","url":null,"abstract":"Acute lung injury (ALI) is a severe inflammatory syndrome characterized by epithelial and endothelial injury, increased pulmonary vascular permeability, and impaired gas exchange. ALI often involves ferroptosis, an iron-dependent form of oxidative cell death. Nuclear factor erythroid 2-related factor 2 (NRF2) is a key regulator of antioxidant defenses, but its role in ALI-related ferroptosis is not well understood. In this study, NRF2 knockout (KO) mice were utilized for transcriptomic analysis to investigate the role of NRF2 in ALI. NRF2 deficiency significantly exacerbated lung injury and ferroptosis, and upregulated the expression of the calcium transporter gene solute carrier family 24 member 2 (SLC24A2). Calcium overload was closely associated with increased SLC24A2 expression and contributed to the development of ferroptosis. These findings were validated in vitro: knockdown of NRF2 in lung epithelial cells enhanced susceptibility to ferroptosis, whereas overexpression of NRF2 attenuated ferroptotic cell death. Conversely, silencing SLC24A2 reduced intracellular calcium overload and suppressed ferroptosis. These results suggest that there may be a regulatory axis between NRF2 and SLC24A2, which has a potential association with inflammation and ferroptosis signals related to acute lung injury (ALI). However, further studies are required to clarify the causal relationship and its consistency across different models, thereby evaluating the feasibility of this axis as a potential therapeutic target.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction: miR-221 Exerts Antiviral and Anti-Inflammatory Effects against HSV-1 Through Direct Repression of CAMK2A and Immune Pathway Activation. 更正：miR-221通过直接抑制CAMK2A和免疫通路激活对HSV-1发挥抗病毒和抗炎作用。

IF 5 2区医学

Inflammation Pub Date : 2026-05-08 DOI: 10.1007/s10753-026-02517-3

Jiahao Xu, Lianhong Xu, Die Hu, Ying Zhang, Yongfang Wang, Zhihua Yun

引用次数: 0

Peripheral Circulating Exosomes Induce Sepsis-associated Liver Injury by Up-regulating STAT1 to Promote Autophagy and Regulating the SLC7A11-GSH-GPX4 Axis to Promote Ferroptosis. 外周循环外泌体通过上调STAT1促进自噬和调节SLC7A11-GSH-GPX4轴促进铁凋亡诱导脓毒症相关肝损伤

IF 5 2区医学

Inflammation Pub Date : 2026-05-02 DOI: 10.1007/s10753-026-02495-6

Yu-Jia Tang, Xue Du, Bing Yin, Hui-Ying Liu, Yi-Jin Tang, Zi-Yue Zhang, Qing-Min Meng, Yan Zhang, Jia-Le Deng, Yao Li, Pei-Lin Yang, Kai Kang, Ming-Yan Zhao, Yang Gao

{"title":"Peripheral Circulating Exosomes Induce Sepsis-associated Liver Injury by Up-regulating STAT1 to Promote Autophagy and Regulating the SLC7A11-GSH-GPX4 Axis to Promote Ferroptosis.","authors":"Yu-Jia Tang, Xue Du, Bing Yin, Hui-Ying Liu, Yi-Jin Tang, Zi-Yue Zhang, Qing-Min Meng, Yan Zhang, Jia-Le Deng, Yao Li, Pei-Lin Yang, Kai Kang, Ming-Yan Zhao, Yang Gao","doi":"10.1007/s10753-026-02495-6","DOIUrl":"https://doi.org/10.1007/s10753-026-02495-6","url":null,"abstract":"Peripheral exosomes have been implicated in the pathogenesis of multiple organ dysfunction during sepsis. However, their role in sepsis-associated liver injury (SALI) remains unclear. This study aimed to investigate the effects of circulating exosomes on hepatic injury and to elucidate the underlying molecular mechanisms of SALI. A murine sepsis model was established via intraperitoneal injection of lipopolysaccharide (LPS). Peripheral exosomes were isolated and co-cultured with murine hepatocytes (AML12 cells). RNA sequencing identified Signal transducer and activator of transcription 1 (STAT1) as a key regulator in exosome-induced liver injury. Since STAT1 functions upstream of the ferroptosis-related solute carrier family 7 member 11 (SLC7A11)-glutathione (GSH)-glutathione peroxidase 4 (GPX4) axis, further in vivo and in vitro experiments were conducted to clarify its mechanistic role. In vitro, exosomes derived from septic mice enhanced inflammatory responses in AML12 cells via STAT1-mediated autophagy and modulation of the SLC7A11-GSH-GPX4 axis, leading to ferroptosis. Inhibition of STAT1 abrogated these effects, whereas STAT1 overexpression potentiated them. In vivo, septic exosomes (sep-Exo) induced liver injury in mice, while suppression of STAT1 abolished the regulatory effects of sep-Exo on ferroptosis, autophagy, and hepatic inflammation. Our findings reveal a novel mechanism underlying SALI, whereby peripheral exosomes upregulate STAT1 to induce autophagy and modulate the SLC7A11-GSH-GPX4 axis, thereby promoting ferroptosis and hepatic inflammation during sepsis.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The miR-155-5p/SOCS1/NF-κB Axis Regulates Airway Smooth Muscle Dysfunction and is a Potential Therapeutic Candidate of Chronic Obstructive Pulmonary Disease. miR-155-5p/SOCS1/NF-κB轴调节气道平滑肌功能障碍，是慢性阻塞性肺疾病的潜在治疗候选者。

IF 5 2区医学

Inflammation Pub Date : 2026-04-27 DOI: 10.1007/s10753-026-02516-4

Kaijun Zhang, Xin Zou, Zhiyi Ma, Weihong Wang, Yongming Wu, Zhaosheng Lin, Machang Luo, Rongzhang Liang, Xiaoming Wu

引用次数: 0

The Histamine Four Receptor Regulates LFA-1 But Not Mac-1 -Dependent Neutrophil Adhesion and Inflammatory Functions. 组胺4受体调节LFA-1但不调节Mac-1依赖性中性粒细胞粘附和炎症功能。

IF 5 2区医学

Inflammation Pub Date : 2026-04-27 DOI: 10.1007/s10753-026-02508-4

Karim Dib

引用次数: 0

Effects of New P2X7R Antagonists on Retinal Inflammatory Degenerative Conditions. 新型P2X7R拮抗剂对视网膜炎性退行性疾病的影响。

IF 5 2区医学

Inflammation Pub Date : 2026-04-25 DOI: 10.1007/s10753-026-02513-7

Chiara Bianca Maria Platania, Federica Conti, Maria Consiglia Trotta, Nicoletta Marchesi, Sonia Panico, Francesca Lazzara, Caterina Claudia Lepre, Marina Russo, Carlo Gesualdo, Francesca Simonelli, Michele D'Amico, Filippo Drago, Alessia Pascale, Settimio Rossi, Valeria Tarallo, Claudio Bucolo

引用次数: 0

MAPK15 Attenuates Intestinal Epithelial Cell Senescence-Like Phenotype to Regulate Gut Homeostasis and Inflammation by Phosphorylating Suz12 to Suppress Drp1-Mediated Mitochondrial Fission Damage. MAPK15通过磷酸化Suz12抑制drp1介导的线粒体裂变损伤，减轻肠上皮细胞衰老样表型，调节肠道稳态和炎症。

IF 5 2区医学

Inflammation Pub Date : 2026-04-24 DOI: 10.1007/s10753-026-02514-6

Juan Li, Gang Chen, Xinyi Bao

引用次数: 0

Dendritic Cells Derived MMP9 Fuels Sepsis-Induced Cardiac Dysfunction Through JNK/AP1 Driven Pro-Inflammatory Cytokine and Nitric Oxide Storm. 树突状细胞衍生的MMP9通过JNK/AP1驱动的促炎细胞因子和一氧化氮风暴促进败血症诱导的心功能障碍。

IF 5 2区医学

Inflammation Pub Date : 2026-04-22 DOI: 10.1007/s10753-025-02374-6

Jiewen Deng, Yulan Qu, Yanyan Jiang, Yao Xie, Xiaotian Ma, Jian Shen, Zhenhong Guo, Meixiang Xiang

引用次数: 0

Dock2 Protects Colitis by Facilitating Akkermansia Colonization via Suppressing IL-22-Reg3 Activity. Dock2通过抑制IL-22-Reg3活性促进Akkermansia定植来保护结肠炎。

IF 5 2区医学

Inflammation Pub Date : 2026-04-22 DOI: 10.1007/s10753-026-02511-9

Min Lu, Shaoting Xu, Ying Tan, Jianping Deng, Bingbing Feng, Ding Qiu, Xinying Wang, Haiyang Sun, Kaile Ji, Bowen Zhu, Shixian Hu, Xueting Wu, Minhu Chen, Yoichiro Iwakura, Xinying Wang, Rui Feng, Yangfan Qi, Ce Tang

引用次数: 0

The Dual Role of Interleukin-10 in Sepsis: Research Progress and Therapeutic Prospects. 白细胞介素-10在脓毒症中的双重作用：研究进展及治疗前景。

IF 5 2区医学

Inflammation Pub Date : 2026-04-22 DOI: 10.1007/s10753-026-02512-8

Xianwen Wang, Qihang Huang, Jinwei Dai, Lina Zhang, Zhaoxin Qian

引用次数: 0