Journal of Inflammation Research最新文献

{"title":"Serum Concentrations of Interleukin-8 and Vitamin D Levels in Jordanian Patients with Rheumatoid Arthritis.","authors":"Ammar Salim Ali Deeb, Seba H Selawi, Kawther Faisal Amawi, Amjad E Hamdallah, Sami Ahmed Zaher Basha","doi":"10.2147/JIR.S509565","DOIUrl":"10.2147/JIR.S509565","url":null,"abstract":"<p><strong>Background: </strong>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation. Vitamin D deficiency and elevated levels of IL-8 have been implicated in the pathogenesis of RA.</p><p><strong>Aims of the study: </strong>This cross-sectional study aims to compare Vitamin D and IL-8 levels between RA patients and healthy controls and assess the relationship between Vitamin D, IL-8, and other inflammatory markers in RA patients.</p><p><strong>Methodology: </strong>The study included 123 participants divided into two groups: 63 RA patients and 60 healthy controls, with equal numbers of males and females in each group. Serum levels of Vitamin D, IL-8, rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibodies, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white blood cell (WBC) count were measured and compared between the groups.</p><p><strong>Results: </strong>RA patients had a higher percentage of females (74.6%) compared to the control group (41.7%). Vitamin D levels were significantly lower in RA patients compared to controls (41.4 ± 25.2 vs 46.5 ± 12.4, p = 0.002). IL-8 levels were significantly higher in the RA group compared to controls (546.9 pg/mL vs 3.1 pg/mL, p < 0.001). RF and anti-CCP antibody levels were also significantly higher in RA patients. However, no significant correlation was found between IL-8, Vitamin D, and other inflammatory markers.</p><p><strong>Conclusion: </strong>The findings highlight the importance of Vitamin D screening or intervention in RA patients due to its potential impact on immune function and disease progression. The elevated IL-8 levels and other inflammatory markers confirm the chronic inflammatory state in RA, emphasizing the need for continuous inflammation-targeted approaches, including pharmacological treatment and lifestyle modifications.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8993-9000"},"PeriodicalIF":4.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626557","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":"Immune Microenvironment Characterization and Machine Learning-Guided Identification of Diagnostic Biomarkers for Ulcerative Colitis.","authors":"Qingqing Zheng, Li Wang, Yu Zhang, Jun Peng, Jianhong Hou, Hui Wang, Yazhe Ma, Peiren Tang, Ying Li, Huan Li, Yun Chen, Jie Li, Yang Chen","doi":"10.2147/JIR.S526325","DOIUrl":"10.2147/JIR.S526325","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) is a chronic inflammatory bowel disease hallmarked by dysregulated immune responses. Current treatments often show limited efficacy, highlighting the need for novel diagnostic and therapeutic approaches.</p><p><strong>Methods: </strong>RNA-Seq data from 495 UC patients and 320 controls (training dataset) and 389 UC patients and 209 controls (testing dataset) were analyzed. Immune cell infiltration was assessed via the ImmuCellAI algorithm, while differential expression analysis and WGCNA were performed to identify key immune-related genes. Moreover, machine learning models, including Random Forest and Best Subset Selection, were used to construct and validate an optimal diagnostic framework. Lastly, the findings were further corroborated using immunohistochemistry conducted on tissue samples from UC patients and controls.</p><p><strong>Results: </strong>Thirteen immune cell types, including B cells, macrophages, and naive CD4+ T cells, were identified as significantly altered in UC. Likewise, cytokines such as IL-10, TGF-β, RORγ, and IL-21 exhibited abnormal expression patterns in UC tissues. WGCNA identified three immune cell-associated gene modules, among which the MEblue, MEturquoise, and MEgrey modules were highly correlated with aberrant immune cells. Additionally, machine learning models identified 99 candidate genes, from which an optimal diagnostic model comprising eight crucial genes (GATA2, IL8, LAT, NOLC1, SMARCA5, SMC3, STX10, ZMIZ1) was constructed, achieving an AUC of 0.964 in the training dataset, 0.926 in the internal test dataset, and 0.884 in the independent test dataset. Functional enrichment analysis revealed associations with inflammatory and immune-regulatory pathways, highlighting their biological relevance. Moreover, the identified eight genes hold translational potential for clinical diagnostics and may serve as a foundation for future precision-targeted therapies in UC.</p><p><strong>Conclusion: </strong>This study highlights alterations in the immune microenvironment in UC and presents an accurate eight-gene diagnostic model, offering the potential for early detection and novel therapeutic targets.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8977-8992"},"PeriodicalIF":4.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637219","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":"Combining Preoperative and Postoperative Prognostic Nutritional Index as an Improved Prognostic Factor for Overall Survival in Patients with Colorectal Cancer.","authors":"Jong Min Lee, Jeonghyun Kang","doi":"10.2147/JIR.S529218","DOIUrl":"10.2147/JIR.S529218","url":null,"abstract":"<p><strong>Purpose: </strong>While preoperative prognostic nutritional index (PNI) is a well-established prognostic marker in colorectal cancer (CRC), and postoperative PNI has gained attention, their combined prognostic value remains largely unexplored.</p><p><strong>Patients and methods: </strong>We analyzed patients who underwent curative surgery for stage I-III CRC between March 2004 and February 2014. The pre- and postoperative PNI, measured within 1 month before and 3-8 weeks after surgery, were combined to create \"change-PNI\" The Cox proportional hazards model was used to assess the prognostic significance, and the C-index was compared across values.</p><p><strong>Results: </strong>The optimal pre- and postoperative PNI cutoff values predicting 5-year overall survival (OS) were 48.05 and 43.65, respectively. The patients were categorized into four groups based on their pre- and postoperative values: pre-low + post-low (G1), pre-low + post-high (G2), pre-high + post-low (G3), and pre-high + post-high (G4). A multivariable Cox proportional hazards model demonstrated that patients in G2, G3, and G4 had significantly lower mortality risks than those in G1 (HR [95% CI] vs G1: G2, 0.341 [0.186-0.625]; G3, 0.457 [0.222-0.941]; G4, 0.222 [0.123-0.401]). The C-index of change-PNI (0.671, 95% CI 0.617-0.720) was superior to that of preoperative PNI (0.609, 95% CI 0.563-0.654) (bootstrap mean difference: 0.062, 95% CI 0.029-0.099) and postoperative PNI (0.622, 95% CI 0.581-0.664) (bootstrap mean difference: 0.049, 95% CI 0.014-0.085).</p><p><strong>Conclusion: </strong>Change-PNI serves as a more effective independent immuno-nutritional marker than pre- or postoperative PNI in predicting OS in patients undergoing surgery for non-metastatic colorectal cancer.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8935-8944"},"PeriodicalIF":4.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626545","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":"Macrophages as Multifaceted Orchestrators of Tissue Repair: Bridging Inflammation, Regeneration, and Therapeutic Innovation.","authors":"Li Wang, Kai Yang, Xinxin Xie, Shaohui Wang, Huiping Gan, Xiaoli Wang, Hailiang Wei","doi":"10.2147/JIR.S527764","DOIUrl":"10.2147/JIR.S527764","url":null,"abstract":"<p><p>Macrophages play pivotal roles in tissue repair through remarkable functional plasticity, orchestrated by their developmental origins and local microenvironmental cues. Embryonically derived resident macrophages primarily maintain tissue homeostasis, while monocyte-derived macrophages respond predominantly to inflammation and extracellular matrix remodeling. Effective tissue repair requires precise temporal regulation of macrophage polarization, balancing inflammation resolution, angiogenesis, and scar formation. Metabolic reprogramming further enhances macrophage plasticity, enabling adaptation to fluctuating energy demands at injury sites. Emerging evidence also highlights that macrophages integrate biomechanical forces-such as matrix stiffness and shear stress-with biochemical signals to fine-tune their inflammatory and reparative programs. Recognizing this mechanoregulation broadens therapeutic avenues for precisely modulating macrophage behavior in regenerative medicine. Targeting macrophage subsets, polarization states, or metabolic pathways has emerged as a promising therapeutic strategy to optimize healing outcomes. However, the inherent complexity of macrophage heterogeneity presents considerable challenges to therapeutic precision. This review systematically summarizes the multifaceted roles of macrophages in tissue repair, emphasizing how developmental origins dictate functional specificity, dynamic phenotypic transitions, and metabolic adaptability, aiming to advance macrophage-based precision therapeutics for regenerative medicine.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8945-8959"},"PeriodicalIF":4.2,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626555","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":"Exploring the Anti-Inflammatory and Anti-NET Properties of Zidian Zhenxiao Granule in IgA Vasculitis: A Network Pharmacology and Proteomic Study.","authors":"Xiaofang Zhang, Minghang Yang, Xiaozheng Duan, Xiaochun Feng, Yanqiu Fang","doi":"10.2147/JIR.S522082","DOIUrl":"10.2147/JIR.S522082","url":null,"abstract":"<p><strong>Background and purpose: </strong>Immunoglobulin A vasculitis (IgAV) is the most common systemic vasculitis of childhood. Zidian Zhenxiao granule (ZDZX), a 9-herb formula optimized through decades of clinical practice, uniquely integrates anti-inflammatory and immunomodulatory properties. However, its mechanisms targeting neutrophil extracellular traps (NETs) and thromboinflammatory pathways in combating IgAV remain unclear. This study aimed to investigate the main component of ZDZX and its underlying mechanism in IgAV treatment.</p><p><strong>Methods: </strong>Combining UHPLC-QE-MS/MS, network pharmacology, 4D-FastDIA proteomics, and a gliadin-induced IgAV murine model, we systematically deciphered ZDZX's renoprotective and anti-inflammatory mechanisms.</p><p><strong>Results: </strong>19 key components were identified in ZDZX, targeting 46 IgAV-associated proteins, predominantly enriched in TNF and IL-17 signaling pathways. In vivo, ZDZX significantly reduced levels of blood urea nitrogen (BUN) and creatinine (<i>p</i> <0.01), attenuated renal IgA/C3 deposition, and improved hematological parameters. Proteomics revealed 27 differentially expressed proteins (DEPs) (FDR <0.05), including MPO, IL-17, MMP2, C3 and COL1A1, implicating coagulation cascades and neutrophil extracellular trap (NET) formation. Additionally, ZDZX downregulated renal IL-6, TNF-α, and citrullinated histone H3 (CitH3) (<i>p</i> <0.01), confirming NET inhibition, consistent with recent IgAV-NET mechanistic studies.</p><p><strong>Conclusion: </strong>By synergizing network pharmacology, 4D-FastDIA proteomics, and experimental validation, this study pioneers the demonstration that ZDZX alleviates IgAV via multi-target inhibition of NET-driven thromboinflammation.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8915-8933"},"PeriodicalIF":4.2,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626546","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":"Metabolomic Profiling Reveals Serum Tryptophan as a Potential Therapeutic Target for Systemic Lupus Erythematosus.","authors":"Kai Wang, Rujie Zhu, Min Xu, Kexin Zhu, Ju Li, Chang Li, Deqian Meng, Hongwei Chen, Lingyun Sun","doi":"10.2147/JIR.S505306","DOIUrl":"10.2147/JIR.S505306","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to identify potential diagnostic biomarkers for systemic lupus erythematosus (SLE) using metabolomics approaches and machine learning algorithms, and to evaluate therapeutic targets for SLE treatment.</p><p><strong>Methods: </strong>Serum samples from 44 SLE patients with lupus nephritis, 40 rheumatoid arthritis patients, 39 primary Sjögren's syndrome patients, and matched healthy controls were analyzed using ultra-performance liquid chromatography-high resolution mass spectrometry (UPLC-HRMS). Eight machine learning algorithms were employed to establish diagnostic models. Partial least squares discriminant analysis (PLS-DA) and orthogonal PLS-DA (OPLS-DA) were used to identify differential metabolites. The therapeutic potential of identified metabolites was validated in MRL-Fas <i>^lpr</i> mice through histological examination, flow cytometry, and biochemical analysis.</p><p><strong>Results: </strong>A total of 129 metabolites were detected, with machine learning models achieving area under the curve (AUC) values >0.8. The principal component regression model performed best with AUC values of 0.99 and 0.96 for training and test datasets, respectively. Two key metabolites, tryptophan and beta-alanine, showed significantly decreased levels in SLE patients compared to healthy controls (both p<0.05), while exhibiting opposite patterns in other autoimmune diseases. In the mouse model, tryptophan supplementation improved renal histology, reduced proteinuria, increased naïve T cells and central memory T cells, and decreased effector T cell frequencies in both peripheral blood and spleen.</p><p><strong>Conclusion: </strong>This study demonstrates the successful application of machine learning algorithms to metabolomics data for SLE classification and identifies tryptophan and beta-alanine as potential SLE-specific biomarkers. Tryptophan supplementation shows therapeutic promise in lupus mouse models through immunomodulatory effects on T cell subsets and renal protection.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8899-8913"},"PeriodicalIF":4.2,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626556","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":"From Microbial Homeostasis to Systemic Pathogenesis: A Narrative Review on Gut Flora's Role in Neuropsychiatric, Metabolic, and Cancer Disorders.","authors":"Xili Yan, Liangbin Shi, Xiuling Zhu, Yingdi Zhao, Jie Luo, Qiang Li, Zhiliang Xu, Jian Zhao","doi":"10.2147/JIR.S531671","DOIUrl":"10.2147/JIR.S531671","url":null,"abstract":"<p><p>As a pivotal ecological regulator in humans, the gut microbiota profoundly participates in the pathological processes of neurodegenerative diseases, psychiatric disorders, metabolic syndromes, and cancers through metabolite exchange, epigenetic regulation, and gut-brain axis signaling. This review focuses on analyzing relationships between gut microbial communities and four major disease spectra: neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, Huntington's disease)-revealing microbiota-derived lipopolysaccharide activation of microglia and gut-brain transmission pathways of α-synuclein; mental health disorders (depression, schizophrenia, bipolar disorder)-elucidating dysregulated tryptophan metabolism and gut-derived neurotransmitter imbalances; metabolic diseases (obesity, diabetes, gout)-analyzing molecular mechanisms by which short-chain fatty acids regulate insulin sensitivity and uric acid metabolism; malignant tumors (lung cancer, breast cancer, prostate cancer)-exploring microbial remodeling of immune checkpoint inhibitor responses and regulatory effects on estrogen metabolism. We integrate existing evidence to systematically expound the roles of gut microbiota alterations in the pathogenesis of neurodegenerative diseases, psychiatric disorders, metabolic dysregulation, and malignant tumors, with in-depth analysis of mechanisms through which dysbiosis promotes disease progression, aiming to provide a theoretical foundation and scientific recommendations for developing microbiota-targeted precision intervention strategies (including, but not limited to synthetic microbial community transplantation and metabolite-directed regulation).</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8851-8873"},"PeriodicalIF":4.2,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600701","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":"Multi-Omics Analysis and Validation of Cell Senescence-Related Genes Associated with Non-Alcoholic Fatty Liver Disease.","authors":"Jianhua Gong, Zhijie Qin, Yihao Xiao, Jixue Li, Qing Wang, Liping Lei, Jiangfa Li","doi":"10.2147/JIR.S525168","DOIUrl":"10.2147/JIR.S525168","url":null,"abstract":"<p><strong>Objective: </strong>To assess causal links between senescence-related genes and non-alcoholic fatty liver disease (NAFLD) using summary-data Mendelian randomization (SMR) and colocalization analyses.</p><p><strong>Methods: </strong>Our study examined the relationship between senescence and NAFLD by integrating DNA methylation, gene expression, and protein quantitative trait loci (mQTL, eQTL, and pQTL) data. Summary statistics for NAFLD were sourced from a previous study (discovery) and the FinnGen database (replication), with additional cohorts for nonalcoholic steatohepatitis and liver fibrosis. Genetic variants near senescence-related genes were used as instrumental variables to assess causal relationships. Colocalization analysis was performed to confirm shared causal variants and liver-specific eQTL data were used for validation. Furthermore, we validated findings using cell and mouse models of NAFLD. Cell models were treated with oleic acid, and NAFLD mice were induced using a high-fat diet.</p><p><strong>Results: </strong>We identified 40 mQTLs, 9 eQTLs, and 3 pQTLs significantly linked to NAFLD in the discovery cohort. Multi-omics data highlighted three genes-<i>S100A6, ENDOG</i>, and <i>TP53I3</i>-as potential causal contributors. Notably, S100A6 was confirmed at both the methylation sites (cg24155129 and cg01910639) and gene expression levels, with methylation at these CpG sites significant regulating its expression. Liver-specific validation revealed that <i>ENDOG</i> expression was negatively associated with NAFLD, consistent with findings in blood. Finally, differential expression of all three genes was confirmed in cell models, with S100A6 and <i>ENDOG</i> further validated in a mouse model.</p><p><strong>Conclusion: </strong>Our findings suggest that <i>S100A6, ENDOG</i>, and <i>TP53I3</i> are associated with NAFLD, providing insights for further research into the disease's underlying etiology.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8821-8833"},"PeriodicalIF":4.2,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600703","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":"Prediction for Acute Biliary Pancreatitis After Laparoscopic Cholecystectomy.","authors":"Dacheng Yue, Shixiang Hu","doi":"10.2147/JIR.S531707","DOIUrl":"10.2147/JIR.S531707","url":null,"abstract":"<p><strong>Background: </strong>Acute biliary pancreatitis (ABP), caused by biliary stones, is a severe inflammatory condition with high mortality rates. ABP recurrence is often linked to gallstones, necessitating effective treatment strategies. Despite recent advancements, the prediction of ABP occurrence following LC continues to present challenges, indicating the need for ongoing research and model refinement.</p><p><strong>Purpose: </strong>This study aims to develop a predictive model for assessing the risk of post- Laparoscopic cholecystectomy pancreatitis in patients with gallstones.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted on 968 patients who underwent LC. The patients were divided into the training set and validation set to develop and validate the predictive model. Demographic, clinical, and laboratory data were collected, and univariate and multivariate logistic regression analyses identified risk factors for ABP. A nomogram was constructed, and model performance was assessed using ROC curves, calibration, and decision curve analysis.</p><p><strong>Results: </strong>The incidence of ABP was 9.07% in the training set and 14.43% in the validation set. Significant predictors of post-LC pancreatitis included baseline APACHE II score, choledocholithiasis, number of intubation attempts, timing of cholecystectomy, and biochemical markers (C-reactive protein, white blood cell, red cell distribution width, D-dimer, neutrophils, triglycerides). The predictive model demonstrated high discriminative ability with a receiver operating characteristic value of 0.949 (training set), of folds 1-5 ranged from 0.855 to 0.962 (5-fold cross-validation), and 0.922, (external validation set). Calibration curves confirmed stable prediction performance, and decision curve analysis indicated high net benefit across a range of threshold probabilities.</p><p><strong>Conclusion: </strong>The developed model effectively predicts the risk of post-LC pancreatitis in patients with gallstones, offering valuable guidance for clinical decision-making. Early identification of high-risk patients could improve treatment outcomes and reduce recurrence rates.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8835-8849"},"PeriodicalIF":4.2,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600704","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":"Mechanisms and Targeted Therapeutic Strategies in Sepsis-Induced Myocardial Dysfunction: The Role of NLRP3 Inflammasome-Mediated Inflammation.","authors":"Yuan-Yuan Yu, Rong Wang, Guo-Qing Chen, Yu-Fang Gui, Juan Ma, Jin-Hai Ma, Shu-Jing Li","doi":"10.2147/JIR.S521655","DOIUrl":"10.2147/JIR.S521655","url":null,"abstract":"<p><p>Sepsis is a systemic inflammatory response syndrome triggered by infection, in which excessive immune responses can lead to multiple organ failure and shock. The heart, as one of the critical target organs in sepsis, is significantly impaired, which substantially increases the risk of mortality. Recent studies have increasingly highlighted the role of dysregulated inflammatory responses in the pathogenesis and progression of sepsis-induced myocardial dysfunction (SIMD). Among the key molecular mechanisms regulating various pathophysiological processes and modulating inflammation is the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3(NLRP3) inflammasome. This study aims to explore the role of the NLRP3 inflammasome in the pathogenesis of SIMD, with a focus on its involvement through pathways such as pyroptosis, oxidative stress, autophagy, mitochondrial damage, exosome release, and endoplasmic reticulum stress in the development of SIMD. Furthermore, the research seeks to uncover the potential key roles of the NLRP3 inflammasome in the underlying pathophysiological mechanisms of SIMD. Finally, the study will investigate NLRP3 inflammasome-based therapeutic strategies for targeting SIMD, providing theoretical support for the development of targeted management for SIMD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8875-8897"},"PeriodicalIF":4.2,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600702","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}