Mediators of Inflammation最新文献

{"title":"<i>Tetrastigma hemsleyanum</i> Diels et Gilg Flavonoids Against Acute Lung Injury Via Block NLRP3 Inflammation.","authors":"Lianghui Zhan, Lingling Li, Xiaojun Wu, Xuechun Jiang, Jie Zhou, Sheng Zhu, Changcheng Shu, Jinbao Pu, Weiqing Liang","doi":"10.1155/mi/2279402","DOIUrl":"https://doi.org/10.1155/mi/2279402","url":null,"abstract":"<p><strong>Background: </strong><i>Tetrastigma hemsleyanum</i> Diels et Gilg (Sanyeqing [SYQ]), a traditional anti-inflammatory herb, has been used to treat respiratory disorders.</p><p><strong>Aims: </strong>To elucidate the mechanism of SYQ flavonoids in mitigating acute lung injury (ALI).</p><p><strong>Materials and methods: </strong>An integrated approach combined network pharmacology, HPLC, lipopolysaccharide (LPS)-induced ALI mouse models, and NOD-like receptor thermal protein domain associated protein 3 (NLRP3)-activated cellular assays (LPS + nigericin). NLRP3 knockdown (siRNA) and molecular docking were employed for mechanistic validation.</p><p><strong>Results: </strong>Network pharmacology and HPLC identified procyanidin B1 and catechin as core active compounds targeting the NLRP3 inflammasome pathway. Animal experiments demonstrated that SYQ flavonoids can significantly alleviate pathological damage to lung tissue, reduce pulmonary edema, and inhibit the expression of pro-inflammatory factors, thereby exerting a protective effect against ALI. Furthermore, SYQ flavonoids exhibited protective effects against ALI by downregulating the expressions of interleukin (IL)-1β, IL-18, NLRP3, ASC, and caspase-1. Notably, when NLRP3 was knocked down using siRNA technology, it had no significant effect on the levels of IL-1β and IL-18, indicating that their therapeutic effects are mediated through the NLRP3 pathway. Finally, molecular docking confirmed that both catechin and procyanidin B1 exhibit strong binding affinities with NLRP3, providing a molecular basis for their targeted inhibition of the NLRP3 inflammasome.</p><p><strong>Conclusion: </strong>SYQ flavonoids alleviate ALI by specifically inhibiting the NLRP3 inflammasome, providing a mechanistic basis for its traditional use in lung inflammation.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"2279402"},"PeriodicalIF":4.2,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12968339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434180","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":"Correction to \"Progesterone Administration Modulates Cortical TLR4/NF-κB Signaling Pathway after Subarachnoid Hemorrhage in Male Rats\".","authors":"","doi":"10.1155/mi/9798459","DOIUrl":"10.1155/mi/9798459","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2011/848309.].</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"9798459"},"PeriodicalIF":4.2,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147378081","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":"Association of BRI With Psoriasis and Mediator Effect of SII: A Study Based on NHANES (2003-2006, 2009-2014).","authors":"Ningxin Zhang, Jiaqi Li, Ping Song","doi":"10.1155/mi/7953174","DOIUrl":"10.1155/mi/7953174","url":null,"abstract":"<p><strong>Background and aims: </strong>The prevalence of psoriasis (Pso), a chronic immune-mediated inflammatory skin disease, is high in patients with obesity. This study investigates the mediating role of the systemic immune-inflammation index (SII) in the association between body roundness index (BRI) and Pso prevalence.</p><p><strong>Methods and results: </strong>This study included 14,669 participants from the National Health and Nutrition Examination Survey (NHANES) (2003-2006, 2009-2014). The presence or absence of obesity was identified using the BRI, and Pso was assessed using the Pso questionnaire. The association of BRI with Pso was explored by weighted multivariate logistic regression analyses and restricted cubic spline (RCS) analyses, and the threshold effect was further examined using two-stage linear regression models. Mediation analyses assessed SII's role in the BRI-Pso association. The Pso group included 445 out of 14,669 participants. Logistic regression analyses indicated a positive association between BRI and Pso after adjusting for potential confounders. RCS analyses showed a nonlinear relation between BRI and Pso (<i>P</i> _nonlinear = 0.018), with a point of inflection at 5.103 (odds ratio [OR] = 1.09, 95% CI: 1.04, 1.14). BRI and Pso were positively correlated on the left side of the point of inflection (OR = 1.25, 95% CI: 1.09, 1.45), whereas such an association was not detected on the right side (OR = 1.04, 95% CI: 0.97, 1.11). Mediation analysis showed SII partially mediated this association, accounting for 9.48% of the effect (<i>p</i> < 0.001).</p><p><strong>Conclusion: </strong>BRI is positively associated with Pso, with SII playing a mediating role. These findings highlight the importance of visceral fat management and SII monitoring in addressing Pso and its metabolic comorbidities.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"7953174"},"PeriodicalIF":4.2,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12966767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147378055","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":"Wenyang Decoction Ameliorates DSS-Induced Ulcerative Colitis by Regulating Macrophage Polarization and the PI3K/AKT/mTOR/HIF-1α Signaling Pathway.","authors":"Shengwei Li, Guanghui Yuan, Chan Chen, Jihong Lu, Xing Zhang","doi":"10.1155/mi/7737168","DOIUrl":"10.1155/mi/7737168","url":null,"abstract":"<p><strong>Aim: </strong>Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal inflammation and epithelial damage. This study aims to investigate the therapeutic effects of Wenyang decoction (WYD) in a dextran sulfate sodium (DSS)-induced UC model and its underlying mechanisms, with a focus on macrophage polarization and the regulation of the PI3K/AKT/mTOR/HIF-1α signaling pathway.</p><p><strong>Methods: </strong>A DSS-induced UC model was established in C57BL/6 mice. Treatment groups received WYD at low (8.25 g/kg/day), medium (16.50 g/kg/day), or high (33.00 g/kg/day) doses, with 5-aminosalicylic acid (5-ASA, 200 mg/kg) as a positive control. Assessments included disease activity index (DAI), colon length, histopathology, and levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and oxidative stress markers (SOD, CAT, and MDA). Mechanisms were probed using western blot, qPCR, immunofluorescence, and flow cytometry to analyze macrophage phenotypes (M1/M2) and key signaling pathway proteins.</p><p><strong>Results: </strong>WYD administration dose-dependently alleviated UC symptoms, significantly mitigating body weight loss, reducing DAI scores, and restoring colon length. Histological analysis revealed improved mucosal integrity and reduced inflammatory infiltration. Quantitatively, WYD significantly suppressed pro-inflammatory cytokines (e.g, IL-1β, IL-6, and TNF-α) and attenuated oxidative stress by enhancing antioxidant enzyme activities (SOD and CAT) and decreasing MDA content. Mechanistically, WYD inhibited M1 macrophage polarization (evidenced by downregulation of inducible nitric oxide synthase [iNOS] and CD16/32) and promoted M2 polarization (upregulation of Arg-1 and CD206). Furthermore, WYD treatment significantly inhibited the activation of the PI3K/AKT/mTOR pathway and its downstream target, HIF-1α, both in vivo and in LPS-stimulated RAW264.7 cells.</p><p><strong>Conclusion: </strong>In summary, our findings indicate that WYD exerts significant therapeutic effects in DSS-induced UC. WYD alleviates intestinal inflammation and injury by reshaping macrophage polarization, attenuating oxidative stress, and modulating the PI3K/AKT/mTOR/HIF-1α signaling pathway. This study provides a potential therapeutic strategy for UC in the future.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"7737168"},"PeriodicalIF":4.2,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12966625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147378092","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":"The Mediating Factor of Immune Cell in the Causal Relationship Between Cardiovascular Disease-Related Plasma Proteins and Parkinson's Disease: A Network Mendelian Randomization Analysis.","authors":"Ruotong Yao, Siyao Chen, Yangguang Lu, Yiquan Li, Bohuai Yu, Yingying Liu, Tingxuan Zhang, Yusheng Zhu, Feng Chen, Yuhan Lin, Yukai Wang, Cai Li","doi":"10.1155/mi/7919308","DOIUrl":"10.1155/mi/7919308","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular diseases (CVDs) and their associated plasma proteins exhibit significant correlations with immunity and Parkinson's disease (PD). However, the specific contributions to the risk of developing PD remain unclear. This study aims to investigate the potential causal relationship between CVD-related plasma proteins and the risk of PD and explore the significant mediating role of immune cell phenotypes.</p><p><strong>Methods: </strong>Using publicly available genetic data, we conducted Mendelian randomization (MR) analysis using the inverse variance weighting method to explore the causal relationship between 83 CVD-related plasma proteins and PD. Various MR analysis models were employed for sensitivity analysis. Concurrently, we utilized bioinformatics methods such as protein-protein interaction networks and pathway enrichment analysis to investigate the potential associations between CVD-related plasma proteins and PD-related genes. Finally, we employed a mediator MR design to identify the mediating effects of 731 immune cell phenotypes in the onset of PD.</p><p><strong>Results: </strong>Elevated levels of Fas cell surface death receptors (<i>p</i> = 0.015) and nerve growth factor (<i>p</i> = 0.026) are associated with a reduced risk of PD, while increased levels of thrombomodulin (<i>p</i> = 0.028) are a risk factor for PD. Four immune phenotypes play a significant mediating role in the association between CVD-related proteins and the pathogenesis of PD. Sensitivity analysis indicates that the results are robust.</p><p><strong>Conclusions: </strong>Our study elucidates the close genetic association between CVD-related plasma proteins and PD and identifies the significant mediating role of immune cells, thereby providing valuable insights for future research and clinical applications.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"7919308"},"PeriodicalIF":4.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12960748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147378114","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":"Circ-Eif3c Carried by M2 Macrophage-Derived Exosomes Mitigates Asthma Progression via miR-15a-5p/GSS/SOCS6 Axis Inhibition.","authors":"Jiaying Yuan, Jiayi Zhao, Xiahui Ge, Xingxing Zhu, Li Li, Haoran Ni, Jian Fan, Yi Zhang, Yahong Sun, Yan Shang","doi":"10.1155/mi/8350424","DOIUrl":"10.1155/mi/8350424","url":null,"abstract":"<p><strong>Background: </strong>In the study, we aimed to uncover potential therapeutic mechanisms concerning M2 macrophage-derived exosomes in asthma.</p><p><strong>Methods: </strong>Exosomes were isolated from M0Φ-Exos and M2Φ-Exos. An ovalbumin (OVA)-induced asthma mouse model or lipopolysaccharide (LPS)-induced alveolar epithelial cells (AECs) were created to unravel the therapeutic mechanisms. High-throughput sequencing was used to search for differentially expressed circRNA. Bioinformation analysis and luciferase report analysis were used to reveal the regulationship among circ-Eif3c, miR-15a-5p, glutathione synthetase (GSS), and suppressor of cytokine signaling 6 (SOCS6).</p><p><strong>Results: </strong>The results showed that M2Φ-Exos suppressed OVA-induced inflammatory cytokine secretion and lung injury in mice. Next-generation sequencing (NGS) showed that circ-Eif3c was upregulated in M2Φ-Exos. Circ-Eif3c downregulation inhibited the therapeutic effect of M2Φ-Exos. Bioinformation analysis confirmed that miR-15a-5p, GSS, and SOCS6 were the downstream targets of circ-Eif3c, which were confirmed by luciferase report analysis. The overexpression of miR-15a-5p or the downregulation of GSS/SOCS6 reversed circ-Eif3c's protective effects on LPS-induced AEC damage. The overexpression of circ-Eif3c increased the therapeutic effect of M2Φ-Exos.</p><p><strong>Conclusion: </strong>In conclusion, circ-Eif3c-enriched M2Φ-Exos attenuated airway remodeling by restoring the function of AECs.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"8350424"},"PeriodicalIF":4.2,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12953728/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355634","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":"The Potential Value of Blood Inflammatory Parameters in Diagnosing the Inflammatory Microenvironment and Predicting Fetal Outcomes in Patients With Intrahepatic Cholestasis of Pregnancy.","authors":"Jianyi Gao, Ling Li, Huan Huang, Jing Chen, Ruirui Dong, Jing Wang, Gaoying Wang, Rong Wang, Yingxian Shi, Linxia Shuang, Xiaojin Yang, Ting Zhang, Liang Luo","doi":"10.1155/mi/2838186","DOIUrl":"10.1155/mi/2838186","url":null,"abstract":"<p><p>Previous studies have indicated that the inflammatory microenvironment in pregnant women may contribute significantly to the development of intrahepatic cholestasis of pregnancy (ICP). However, the exact relationship between inflammatory blood parameters and ICP remains uncertain. This study aims to explore the relationship between serum inflammatory factors, inflammatory scoring indicators, and adverse pregnancy outcomes in ICP. Serum samples were collected after 25 weeks of gestation from women clinically diagnosed with ICP, as well as from gestational age-matched healthy pregnant controls. Cytokine levels were subsequently measured using flow cytometry. Correlation analysis was conducted to explore potential relationships between blood inflammatory parameters and other ICP-related markers. Receiver operating characteristic (ROC) curves were generated to evaluate their predictive performance for adverse pregnancy outcomes. Mendelian randomization (MR) analysis was performed to examine potential causal links between inflammation and ICP development. The results revealed significant differences in serum levels of interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) between ICP patients and healthy controls. Additionally, inflammatory scoring indicators were significantly elevated in ICP patients. Most inflammatory parameters correlated with liver function indices and showed positive associations with total bile acids (TBAs). ROC analysis demonstrated that combining inflammatory markers with TBA improved the predictive accuracy for preterm birth (area under the ROC curve [AUC]: 0.865) and low fetal weight (AUC: 0.916). MR analysis identified interleukin-2 (IL-2) and TNF-α as potential risk factors for ICP. Based on these findings, blood inflammatory parameters may serve as accessible and cost-effective indicators for understanding the inflammatory microenvironment in ICP and predicting fetal outcomes.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"2838186"},"PeriodicalIF":4.2,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348658","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":"The TWEAK-HOIP-HuR Axis: A Novel Mechanism of AMPK Inactivation and Metabolic Reprogramming in Lupus Nephritis Mesangial Cells Hyperproliferation.","authors":"Zongnan Ding, Enzhuo Liu, Xinyue Li, Yujie Zhang, Lei Li, Chenghua Weng, Zhiqin Liu, Zhichun Liu","doi":"10.1155/mi/4149395","DOIUrl":"10.1155/mi/4149395","url":null,"abstract":"<p><p>Cellular proliferation is intrinsically coupled to metabolic reprogramming, a conserved biological association that modulates the progression of diverse proliferative pathologies. In the present study, we unveil a novel mechanistic link between tumor necrosis factor-like weak inducer of apoptosis (TWEAK) signaling and Human antigen R (HuR)-driven metabolic alterations in lupus nephritis (LN), a progressive renal disorder characterized by mesangial cells (MCs) hyperproliferation and glomerular dysfunction. We demonstrate that TWEAK stimulation elicits linear ubiquitination of AMP-activated protein kinase (AMPK)-a master regulator of cellular energy metabolism-mediated by the E3 ubiquitin ligase HOIL-1-interacting protein (HOIP). This posttranslational modification directly results in the functional inactivation of AMPK. Notably, suppressed AMPK activity drives the nuclear export of HuR, a ubiquitously expressed RNA-binding protein, leading to its subsequent accumulation in the cytoplasmic compartment. In the cytosol, HuR selectively binds to and stabilizes the mRNAs of key cell cycle regulators, with Cyclin D1 being a primary target. This stabilization of Cyclin D1 mRNA ultimately promotes aberrant MCs proliferation, a pathological hallmark of LN. To validate the functional relevance of the pathogenesis, we performed HOIP knockdown experiments in MCs. Consistent with our mechanistic model, HOIP depletion significantly restored AMPK phosphorylation (a well-established surrogate marker of AMPK activation), suppressed HuR cytoplasmic shuttling, reduced Cyclin D1 expression at both the transcriptional and translational levels, and ultimately inhibited aberrant MCs proliferation in vitro. Collectively, our results establish the TWEAK-HOIP-AMPK-HuR axis as a critical signaling axis that couples metabolic dysfunction to dysregulated cell cycle progression in LN. This work not only provides critical new mechanistic insights into the pathogenesis of mesangial hyperproliferation in LN but also highlights potential therapeutic targets, including HOIP and cytoplasmic HuR, for the development of targeted treatments for LN and other renal diseases characterized by abnormal MCs proliferation.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"4149395"},"PeriodicalIF":4.2,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348675","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":"TUG1 and H19 lncRNAs Can Predict Anti-TNF Unresponsiveness in Patients With Ulcerative Colitis: A Machine Learning-Based Approach.","authors":"Raheleh Heydari, Mohammad Javad Tavassolifar, Mohammad Hossein Derakhshan Nazari, Romina Roshannia, Shabnam Shahrokh, Maryam Parvizi, Mohammad Tayefeh Norooz, Anna Meyfour","doi":"10.1155/mi/9078048","DOIUrl":"10.1155/mi/9078048","url":null,"abstract":"<p><p>The present study aimed to explore the association of long noncoding RNAs (lncRNAs) with inflammation, disease activity, and predicting response to anti-tumor necrosis factor (TNF)-α therapy in patients with ulcerative colitis (UC). Whole blood samples and inflamed biopsies were collected from 42 UC patients at baseline (W0) and week 14 (W14) after receiving anti-TNF treatment as a discovery cohort. Colonoscopy images, histopathological, and clinical symptoms were used to monitor disease activity and response to treatment. LncRNA expression analysis showed increased expression of H19 in the active lesions of UC nonresponders (UCNs) compared to UC responders (UCRs) at baseline, whereas taurine upregulated gene 1 (TUG1) expression was lower. Higher expression of H19 in UCN compared to UCR was still observed at W14, whereas its expression was downregulated in UCR in the remission phase at W14 versus W0, suggesting it as a marker for monitoring disease activity. Moreover, colonic expression of H19 was positively correlated with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). In blood, both H19 and TUG1 showed increased expression in UCN versus UCR at baseline and W14. Three-fold cross-validation-based machine learning approach and receiver operating characteristic (ROC) curve analysis showed that H19 and TUG1 had strong predictive performance for anti-TNF response, with accuracies of 90% and 93% in tissue and 85% and 60% in blood, respectively. In the validation cohort (12 UCR and 10 UCN), expression patterns were reproduced, and predictive performance remained high. H19 showed better accuracy in blood (85%) than tissue (70%), while TUG1 performed best in tissue (92%) and also remained highly accurate in blood (94%). The distinct expression of lncRNAs showed that they could play an important role in the response of UC patients to treatment. They can be a potential biomarker to monitor disease activity and predict response to anti-TNF treatment in UC patients.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"9078048"},"PeriodicalIF":4.2,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12949365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326633","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":"Imidazole Propionate Induces Kidney Damage by Activating the ROS-NLRP3 Signaling Pathway Through mTOR Inhibition of Autophagy in Renal Tubular Epithelial Cells.","authors":"Chen Zeng, Yu-Ru Xiao, Si-Qing Li, Man Guo, Qi Wu, Yi-Meng He, Yu-Fan Zhang, Xiao-Zhen Tan, Yong Xu, Fang-Yuan Teng","doi":"10.1155/mi/2457371","DOIUrl":"10.1155/mi/2457371","url":null,"abstract":"<p><p>L-Histidine, a parent structure of environmental contaminants (e.g., pesticides and preservatives), may undergo bioaccumulation through the food chain and be metabolized by the gut microbiota into deleterious compounds, ultimately compromising human health. Recent studies have identified abnormally elevated levels of the histidine-derived metabolite imidazole propionate (ImP) in the serum of type 2 diabetes mellitus patients. However, the pathophysiological implications of excessive ImP on renal function and its underlying molecular mechanisms remain poorly characterized. This study is the first to elucidate the detrimental effects of ImP on renal function in mice and its molecular mechanisms. Our findings demonstrate that ImP exacerbates renal dysfunction and induces structural and functional abnormalities in renal tubules. Mechanistically, ImP significantly suppresses autophagy in renal tubular epithelial cells and activates the reactive oxygen species (ROS)-NOD-like receptor pyrin domain-containing 3 (NLRP3) signaling pathway, thereby promoting the expression of the pro-inflammatory cytokine interleukin-1β (IL-1β). Notably, the mechanistic target of rapamycin (mTOR) inhibitor rapamycin (Rap) restores autophagy, inhibits the ROS/NLRP3/IL-1β axis, and mitigates ImP-induced renal injury. Transcriptomic sequencing of mouse kidneys reveals that ImP upregulates the expression of autophagy- and inflammation-related genes, while its inhibitor suppresses these genetic alterations. This study highlights the potential nephrotoxic effects of ImP and underscores the therapeutic value of Rap, providing a theoretical foundation for understanding the role of gut microbiota metabolites in the pathogenesis, prevention, and treatment of kidney diseases.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2026 ","pages":"2457371"},"PeriodicalIF":4.2,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12949363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326648","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}