Journal of Inflammation Research最新文献

{"title":"Relationship Between Lymphocyte-Associated Inflammatory Markers and Post-Stroke Cognitive Impairment.","authors":"Qian-Ying Hu, Juan Liu, Cai-Hong Cui, Mei-Fang Guo, Yu-Tong Shi, Xiao-Man Zhang, Bing-Fei Jia, Xin-Yu Li, Su-Juan Sun","doi":"10.2147/JIR.S545953","DOIUrl":"10.2147/JIR.S545953","url":null,"abstract":"<p><strong>Objective: </strong>To determine whether differences in lymphocyte-related inflammatory markers in the ultra-early phase of stroke (within 24 hours of onset) are associated with post-stroke cognitive impairment in the early recovery phase (within 30 days of stroke onset), and to further assess the predictive value of these markers.</p><p><strong>Methods: </strong>The study population consisted of patients who underwent rehabilitation treatment at the Rehabilitation Department of Hebei University Affiliated Hospital between December 2024 and June 2025, within 30 days of stroke onset, ie, during the early recovery phase of stroke. Patients were grouped based on whether they developed cognitive impairment. A retrospective analysis was conducted of patients' blood markers and neurological deficit scores within 24 hours of stroke onset to examine the relationship between ultra-early blood markers and neurological deficits and post-stroke cognitive impairment.</p><p><strong>Results: </strong>There were no significant differences in baseline data between the two groups. However, the proportion of hemorrhagic stroke patients was significantly higher in the PSCI group than in the non-PSCI group (39.7% vs 18.8%, P=0.026<0.05). NLR and NIHSS scores showed significant differences between the two groups. Multivariate analysis indicated that NIHSS (OR=1.297, 95% CI: 1.167-1.442, p<0.001) was independently associated with PSCI, while NLR (OR=1.107, 95% CI: 0.995-1.231, p=0.063) showed a borderline association with PSCI. MLR showed differences between the two groups in univariate analysis (P=0.018) but was excluded in multivariate analysis. ULR did not show significant differences.</p><p><strong>Conclusion: </strong>NIHSS is a strong predictive factor (P < 0.05), with a cut of value of 12 calculated by the ROC curve. NLR is at the threshold for an independent risk factor. Subsequent ROC curves indicate that NLR has low diagnostic sensitivity but high specificity, making it more suitable for screening rather than diagnostic use. MLR and ULR did not demonstrate high predictive value; further studies should be conducted to expand the sample size, perform subgroup analyses, and increase follow-up.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13347-13358"},"PeriodicalIF":4.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12478212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating Pre- and Postoperative Systemic Inflammatory Markers for Acute Kidney Injury Prediction Following Radical Cystectomy: A Multi-Center Retrospective Study.","authors":"Zhongqi Liu, Peng Fan, Yanan Lu, Minghui Cao, Weifeng Yao, Dongtai Chen, Fengtao Ji","doi":"10.2147/JIR.S529335","DOIUrl":"10.2147/JIR.S529335","url":null,"abstract":"<p><strong>Purpose: </strong>The present study aimed to investigate the association of perioperative dynamic changes of systemic inflammation markers with AKI after radical cystectomy and their predictive value through machine learning algorithms.</p><p><strong>Patients and methods: </strong>Patients undergoing radical cystectomy with urinary diversion for bladder cancer from 2013 to 2022 at three university-affiliated tertiary hospitals were gathered. Perioperative dynamic changes of systemic inflammatory markers were calculated based on peripheral blood cell counts from pre- and post-operative values and categorized using restricted cubic splines (RCS). The number of positive changes in these markers was recorded as the perioperative inflammation index. Multivariable logistic regression was utilized to identify risk factors for AKI after radical cystectomy. AKI prediction models were constructed through various supervised machine learning algorithms and evaluated by the area under the receiver operating characteristic curve (AUROC).</p><p><strong>Results: </strong>727 patients were finally enrolled in the study, with 151 (20.8%) patients experiencing AKI following radical cystectomy. Postoperative hemoglobin (p = 0.003; OR, 0.977; 95% CI, 0.962-0.992), albumin level (p = 0.007; OR, 0.906; 95% CI, 0.843-0.974), intraoperative fluid infusion rate (p < 0.001; OR, 0.769; 95% CI, 0.665-0.890) and the perioperative inflammation index (p < 0.001; OR, 1.507; 95% CI, 1.209-1.877) were identified as independent risk factors with predictive value for AKI following radical cystectomy with urinary diversion. Among various machine learning models, XGBoost performed best (AUROC: 0.801; 95% CI: 0.735-0.867) in AKI prediction.</p><p><strong>Conclusion: </strong>The association between perioperative dynamic changes of inflammatory markers and AKI after radical cystectomy reinforced the necessity of perioperative inflammatory evaluation. AKI predictive models, integrating perioperative metrics, enable early identification and optimize perioperative management for AKI prevention.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13335-13345"},"PeriodicalIF":4.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12478227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Validate the Treatment of Crohn's Disease with Chaihu Guizhi Decoction Through Network Pharmacology, Molecular Dynamics Simulation, and in vivo Experiments.","authors":"Weiguo Zhou, Yuguang Wu, Jianhua Yang, Yogesh Kumar Saini, Rui Fu, Bo Chen, Guodong Cao, Jiawei Zhang","doi":"10.2147/JIR.S544465","DOIUrl":"10.2147/JIR.S544465","url":null,"abstract":"<p><strong>Objective: </strong>Using an integrated strategy combining network pharmacology, molecular dynamics simulations, and in vivo experiments, this study explores the stage-specific targets of Chaihu Guizhi Decoction (CGD) for the treatment of Crohn's disease (CD).</p><p><strong>Methods: </strong>First, through the GEO database, the patients with Crohn's disease were divided into four groups: early patients (NCD), late patients (LCD), patients with postoperative recurrence (PCD) and patients without postoperative recurrence (UPCD), and the differential genes of each group were screened. Active ingredients in Chaihu Guizhi Decoction (CGD) with an oral bioavailability (OB) greater than 30% and drug-likeness (DL) exceeding 0.18 were screened using the TCMSP database, along with their corresponding potential targets. The target of CGD was intersected with four groups of differential genes. The common therapeutic targets of CGD for Crohn's disease in four groups and the specific therapeutic targets of each group were obtained. Core targets were identified through protein-protein interaction (PPI) network analysis. The potential mechanism of CGD in treating Crohn's disease was analyzed by enrichment of KEGG and GO. Finally, molecular docking and molecular dynamics simulation were used to verify the possibility of combining the effective ingredients of CGD with the therapeutic target of Crohn's disease. Construct a mouse model of inflammatory bowel disease and administer drug treatment. Use mouse intestinal tissue for Elisa, HE staining, and AB-PAS staining to validate the potential of drug therapy for inflammatory bowel disease. Meanwhile, Western blot experiments were conducted to verify the effect of quercetin on the expression of downstream target proteins.</p><p><strong>Results: </strong>Through molecular docking verification, quercetin can bind to these six core genes. We analyzed quercetin and six gene protein products through molecular dynamics simulation. We found that the complex of quercetin and PTGS2 protein is relatively stable, which may be a therapeutic target. In animal studies, both CGD and quercetin significantly alleviated inflammation-induced intestinal shortening (p < 0.05). ELISA results demonstrated that CGD and quercetin markedly reduced the expression of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α (p < 0.05). Furthermore, histopathological examinations via HE and PAS staining revealed a substantial mitigation of intestinal inflammation following treatment with CGD and quercetin.</p><p><strong>Conclusion: </strong>This study found through animal experiments that CGD and quercetin can treat CD. Through network pharmacology, molecular dynamics simulations, and Western blot experiments, it was demonstrated that quercetin can treat inflammatory bowel disease by affecting the expression of PTGS2 and IL-1B proteins.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13235-13254"},"PeriodicalIF":4.1,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Focus on the Mechanisms of Alteration in Host Lymphocyte Level Following Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) Infection.","authors":"Yundi Chen, Heather Miller, Kamel Benlagha, Maria G Byazrova, Alexander V Filatov, Ziyin Zhang, Lian Liu, Yan Ding, Lu Yang, Quan Gong, Chaohong Liu","doi":"10.2147/JIR.S531068","DOIUrl":"10.2147/JIR.S531068","url":null,"abstract":"<p><p>Nowadays, severe fever with thrombocytopenia syndrome (SFTS), featuring clinical manifestation of fever with leukopenia, thrombocytopenia and multiple organ function impairment, has been paid more and more attention. It has become the pandemic for a few years and a quantity of people died of it. Severe fever with thrombocytopenia syndrome virus (SFTSV) infection may lead to the development of SFTS, which is characterized by decreased counts of lymphocyte subsets, especially T cells, B cells and natural killer cells, and disruptive release of cytokines, chemokines and growth factors. However, the deeper mechanism of this disease remains unidentified. To excavate the mechanisms of lymphopenia in SFTSV infection and to introduce the potential therapeutics, this paper focuses on lymphopenia as well as reviews the mechanisms and effects of lymphopenia caused by SFTSV infection, mainly through making analogies with other similar viruses to explain the details of programmed cell death. Other factors such as IL-6,IL-10, TNF-α and some vital immunocytes also play significant roles in eliciting lymphopenia. Eventually, the probable clinical implications have been discussed, mentioning that lymphopenia induced by multiple pathways in SFTSV infection may be associated with the severity of viral disease and opportunistic infection.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13265-13277"},"PeriodicalIF":4.1,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between High-Sensitivity C-Reactive Protein and Longitudinal Changes in Arteriosclerosis Over Time: The Kailuan Prospective Cohort Study.","authors":"Weizhe Li, Pei Liang, Zhao Han, Xiaohui Liu, Shasha An, Xin Wang, Yanling Gao, Shuohua Chen, Shouling Wu","doi":"10.2147/JIR.S541222","DOIUrl":"10.2147/JIR.S541222","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the relationship between high-sensitivity C-reactive protein (hs-CRP) and the longitudinal changes in arterial Arteriosclerosis over time.</p><p><strong>Methods: </strong>Using a prospective cohort study design, 25,336 participants from the Kailuan study cohort, who had completed at least two baPWV measurements and met the inclusion criteria, included in the analysis. Participants were divided into three groups based on baseline hs-CRP levels: hs-CRP<1 mg/L, 1 mg/L≤hs-CRP≤3 mg/L, and hs-CRP >3 mg/L. The relationship between hs-CRP and the longitudinal changes in baPWV was analyzed using a linear mixed-effects model.</p><p><strong>Results: </strong>(1) The average follow-up duration was 4.62 ± 2.86 years. At the end of the follow-up, the baPWV of the three groups:hs-CRP < 1 mg/L (n=11,651), 1 mg/L ≤ hs-CRP ≤ 3 mg/L (n=9,369), and hs-CRP > 3 mg/L (n=4,316) increased over time. The average rate of increase in baPWV was 84.26 cm/s, 88.06 cm/s, and 73.92 cm/s, respectively. (2) The linear mixed-effects model analysis of factors affecting the progression of Arteriosclerosis, after adjusting for confounding factors, showed that compared to the hsCRP_1 group, the baPWV increase rate in the hsCRP_2 and hsCRP_3 groups was progressively higher. The effect Estimate were 14.4 cm/s (95% CI 6.54 to 22.34, <i>P</i><0.001) and 40.67 cm/s (95% CI 5.28 to 51.02, <i>P</i><0.001), respectively. Stratifying by gender showed that the impact was more pronounced in males, with effect Estimate of 20.56 cm/s (95% CI 6.18 to 8.45, <i>P</i><0.001) and 43.06 cm/s (95% CI 27.82 to 58.31, <i>P</i><0.001), respectively. Sensitivity analysis confirmed that this longitudinal association was more pronounced.</p><p><strong>Conclusion: </strong>There is a significant \"dose-response\" relationship between hs-CRP and the longitudinal progression of Arteriosclerosis, with a more pronounced effect observed in the male population.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13255-13264"},"PeriodicalIF":4.1,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiome-Gut-Brain Axis: Implications for the Links Between Inflammatory Bowel Disease and Neuropsychiatric Disorders.","authors":"Cheng-Mei Tian, Mei-Feng Yang, Chen Kong, Duo Luo, Ning-Ning Yue, Hai-Lan Zhao, Yuan Zhang, Jian-Ping Lu, Yu-Jie Liang, Yang Song, Dao-Ru Wei, Jun Yao, Li-Sheng Wang, De-Feng Li","doi":"10.2147/JIR.S514838","DOIUrl":"10.2147/JIR.S514838","url":null,"abstract":"<p><p>The brain and gastrointestinal tract are closely interconnected as important sensory organs processing signals from both environmental and internal cues. Recent studies have shown that dysregulation of the gut microbiota in inflammatory bowel disease activates the gut immune system. The cross-talk mechanism along the gut-brain axis is implicated in the development of neuropsychiatric disorders such as autism, depression, anxiety, Alzheimer's disease, and Parkinson's disease. Here, we discuss the molecular mechanisms involved in signaling across the gut-brain axis, including the immune and neuroendocrine system, intestinal permeability, microbial composition, and bacterial extracellular vesicles. We focus on the link between specific inflammatory bowel disease, microbial genera and psychiatric and neurological disorders, and propose that the results of preclinical and clinical studies open up the possibility of targeting the gut microbiota to treat neuropsychiatric disorders that are altered by gut interactions.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13183-13212"},"PeriodicalIF":4.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying Chemokine System-Related Phenotype to Predict Immune Feature in Pan-Cancer and Prognostic Signature for Lung Adenocarcinoma.","authors":"Tianming Zhao, Xu Wu, Shiqi Guo, Jun Nie, Shitao Fang, Liangchao Wang, Xiaojuan Li, Tingting Nie, Kecheng Yao, Xinge Du, Yingnan Wang, Yurong Yuan, Jixiang Ni","doi":"10.2147/JIR.S537256","DOIUrl":"10.2147/JIR.S537256","url":null,"abstract":"<p><strong>Background: </strong>The chemokine system modulates tumor cell characteristics and influences immune cell function. This research investigates the roles of chemokines and their receptors (CaCRs) across multiple cancers and establishes a reliable CaCRs-based prognostic model for lung adenocarcinoma (LUAD).</p><p><strong>Methods: </strong>Gene expression data were sourced from the UCSC-Xena platform and the GEO database. The chemokine score was calculated using the ssGSEA algorithm. A CaCRs-based prognostic signature was constructed and validated for LUAD. Expression levels of signature genes in lung cancer tissues were verified.</p><p><strong>Results: </strong>Dysregulation of CaCRs expression was observed in multiple cancers. The chemokine score has shown prognostic features in various tumors. In the LUAD cohort, a seven-gene signature of CaCRs (CCR2, CCR4, CCR6, XCR1, CCL20, CXCL17, and XCL2) was constructed as a prognostic model, identifying a poorer prognosis for high-risk groups. mRNA levels of CCR2, CCR4, CCR6, and XCR1 were significantly reduced in lung cancer tissues compared to adjacent normal tissues, while CCL20 was markedly overexpressed in tumor tissues. Furthermore, CCL20 promoted A549 cell proliferation via the MAPK pathway, with JNK inhibitors effectively blocking CCL20-induced proliferation.</p><p><strong>Conclusion: </strong>This study highlights the substantial role of CaCRs in immunity and prognosis. The identified seven-gene signature of CaCRs provides a new prognostic tool for LUAD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13213-13234"},"PeriodicalIF":4.1,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12475510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Emerging Roles and Therapeutic Potential of Unconventional T Cells in Sepsis.","authors":"Shuaipeng Gu, Peidong Zhang, Cong Zhang, Tingxuan Tang, Teding Chang, Liming Dong, Wei Gao, Zhaohui Tang","doi":"10.2147/JIR.S545532","DOIUrl":"10.2147/JIR.S545532","url":null,"abstract":"<p><p>Sepsis represents a dynamic, dysregulated host immune response to infection in which unconventional T cells-γδ T cells, mucosal-associated invariant T (MAIT) cells, natural killer T (NKT) cells, and double-negative T cells-actively shape the balance between early hyperinflammation and subsequent immune paralysis across time and tissues. These cells employ unique antigen recognition mechanisms to trigger rapid immune responses. γδ T cells facilitate early pathogen elimination and immune regulation, whereas MAIT cells detect microbial metabolites and modulate the systemic inflammation. NKT cells balance immune homeostasis through dual pro- and anti-inflammatory cytokine production. This review classifies these subsets and examines their sepsis-related functions alongside immunotherapies targeting them, such as cytokine manipulation, immunomodulators, and checkpoint inhibitors. Elucidating the precise mechanisms underlying sepsis could advance therapies that restore immune equilibrium and potentially improve clinical outcomes. Future studies should unravel the interactions between unconventional T cells and broader immune networks while translating the findings into practical treatments. Understanding the dynamic roles of these cells provides pathways for tailored interventions in sepsis management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13139-13157"},"PeriodicalIF":4.1,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic Value and Regulatory Mechanism of miR-322-5p in Coronary Heart Disease.","authors":"Mingyang Wang, Jing Wang, Yanan Xie","doi":"10.2147/JIR.S536945","DOIUrl":"10.2147/JIR.S536945","url":null,"abstract":"<p><strong>Background: </strong>Coronary heart disease (CHD) is a heart condition caused by narrowed or blocked coronary arteries. The miR-322-5p is closely related to inflammation and vascular diseases, yet its role in CHD remains unknown.</p><p><strong>Objective: </strong>This study focused on investigating the clinical significance of miR-322-5p and its regulatory mechanism in CHD.</p><p><strong>Materials and methods: </strong>This study enrolled 160 CHD patients and 130 healthy individuals. The expression of miR-322-5p and TRAF6 was measured by RT-qPCR. The correlation between miR-322-5p and CHD was evaluated via Pearson correlation analysis. The clinical predictive performance of miR-322-5p was assessed by ROC analysis. Cell viability was assessed using the CCK-8 assay while apoptosis was analyzed by flow cytometry. Inflammatory cytokine levels were determined by ELISA.</p><p><strong>Results: </strong>MiR-322-5p was significantly downregulated in patients with CHD and exhibited high diagnostic accuracy for CHD with an AUC of 0.882. The declined miR-322-5p was negatively correlated with Gensini score (r = -0.611) and CRP (r = -0.646), but positively associated with HDL-C (r = 0.598). Although miR-322-5p was reduced under pathological conditions, its upregulation enhanced cell viability and inhibited both apoptosis and inflammatory factors. TRAF6, a direct target of miR-322-5p, was negatively regulated by miR-322-5p (r = -0.683), and high levels of TRAF6 aggravated CHD.</p><p><strong>Conclusion: </strong>The declined miR-322-5p in CHD presented high diagnostic value. Reduced miR-322-5p exacerbated the CHD by inhibiting cell viability, enhancing apoptosis and inflammation through negatively regulating the TRAF6.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13173-13182"},"PeriodicalIF":4.1,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12460061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial Injury-Induced Shedding of Thrombomodulin as a Biomarker for Predicting Adverse Prognosis in Sepsis.","authors":"Xinmeichen Meng, Xuemei Chen, Jiwen Liu, Xiaoyan Yuan, Dongfeng Guo","doi":"10.2147/JIR.S535854","DOIUrl":"10.2147/JIR.S535854","url":null,"abstract":"<p><strong>Purpose: </strong>Sepsis-associated endothelial injury drives thrombomodulin (TM) shedding and severe coagulopathy. We hypothesized that plasma TM levels predict sepsis severity and prognosis. This study investigated the prognostic association of plasma TM as a sepsis biomarker and validated it in a murine model.</p><p><strong>Patients and methods: </strong>In a prospective cohort (Gongli Hospital, Shanghai; July 2024-January 2025), 68 sepsis patients (45 survivors, 23 nonsurvivors) and 50 controls underwent plasma TM, CD64 index, procalcitonin (PCT), C-reactive protein (CRP), Sequential Organ Failure Assessment (SOFA) score, and Acute Physiology and Chronic Health Evaluation II (APACHE II) score assessments. Survival analysis, multivariable regression, and receiver operating characteristic (ROC) curve modeling were performed. Mechanistic validation utilized Cecal Ligation and Puncture (CLP) mice with plasma/aortic TM quantification.</p><p><strong>Results: </strong>Elevated plasma TM and CD64 index correlated with poor prognosis (<i>p</i><0.05). The combined TM/CD64 Index ROC model achieved superior predictive performance (AUC=0.9671, <i>p</i><0.05) compared with TM alone (AUC=0.9333) or CD64 alone (AUC=0.8628). The multiple linear regression model indicated a positive correlation between TM levels in sepsis patients and SOFA and APACHE II scores. In vivo, experiments indicate plasma TM increased while aortic endothelial TM expression decreased.</p><p><strong>Conclusion: </strong>This study demonstrates that the combined plasma TM and CD64 index assessment enhances early prediction of adverse sepsis outcomes, with strong correlations to clinical severity scores. The paradoxical TM dynamics (plasma elevation vs endothelial depletion) suggest endothelial injury as a key mechanism. Future research should focus on multicenter validation, and mechanistic studies are warranted to optimize clinical translation.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"13055-13072"},"PeriodicalIF":4.1,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}