Journal of Inflammation Research最新文献

{"title":"Exploring the Pleiotropy of PCSK9: A Wide Range of Influences from Lipid Regulation to Extrahepatic Function.","authors":"Huaru Wang, Guodong Tang, Jianqiang Wu, Xuzhen Qin","doi":"10.2147/JIR.S509222","DOIUrl":"https://doi.org/10.2147/JIR.S509222","url":null,"abstract":"<p><p>In cardiovascular disease, the discovery of the proprotein convertase subtilisin/kexin type 9 (PCSK9) has undoubtedly opened a new chapter in regulating blood lipids. Since its first identification as a key regulator of low-density lipoprotein receptor (LDLR) degradation in 2003, the role of PCSK9 in cholesterol metabolism has been extensively studied. However, with further research, the pleiotropy of PCSK9 has gradually emerged, and its impact extends far beyond cholesterol metabolism in the liver. The purpose of this review is to systematically explore the pleiotropy of PCSK9, extending from its important role in lipid regulation to its extensive effects in extrahepatic tissues, and to reveal its potential role in cardiovascular health, nervous system function, and tumor biology. By integrating the latest research findings, this paper summarizes the complex mechanisms of action of PCSK9 in different biological processes and explores its potential and challenges as a therapeutic target.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4509-4532"},"PeriodicalIF":4.2,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780349","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":"Recent Advances of Type I Interferon on the Regulation of Immune Cells and the Treatment of Systemic Lupus Erythematosus.","authors":"Xiaocui Wang, Bin Wen, Xuemei Duan, Yunfei Zhang, Ying Hu, Haonan Li, Huifeng Shang, Yukai Jing","doi":"10.2147/JIR.S516195","DOIUrl":"https://doi.org/10.2147/JIR.S516195","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with multiple organ damage. Several studies have found that, in addition to significant production of autoantibodies, the majority of SLE patients exhibit increased expression of type I interferon (IFN-I) regulated genes (also known as IFN-I traits), and that IFN-I plays a crucial role in the pathogenesis of SLE. In SLE, virtually all immune cells are dysregulated, and most of these aberrant dysregulations are directly or indirectly affected by IFN-I. The mechanism of action of IFN-I in these immune cells is multifaceted. In this review, we focus on the immune cell types that produce IFN-I and are affected by IFN-I in SLE. Importantly, we explore the research progress of related drugs in terms of IFN-I production, itself, and downstream. Here we provide the most up-to-date information on the mechanisms that lead to the pathogenesis of SLE, providing the basis for the development of innovative future therapies and future research directions.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4533-4549"},"PeriodicalIF":4.2,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780352","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":"Experimental Liver Surgery for Liver Research: Update, Choice and Translation.","authors":"Ji-Hua Shi, Pål-Dag Line, Shui-Jun Zhang, Wen-Zhi Guo","doi":"10.2147/JIR.S506737","DOIUrl":"10.2147/JIR.S506737","url":null,"abstract":"<p><p>Experimental animal models of liver surgery are crucial for understanding human liver physiology and pathogenesis and identifying novel therapeutic modalities for liver disease. Herein, we update the brief summary of the most widely used experimental models and concepts in hepatic surgery, including hepatic ischemia/reperfusion, partial hepatectomy, liver transplantation, techniques and parameters of vascular perfusion of the liver, and using bile duct ligation as a model of cholestasis for the development of liver fibrosis. We focus on surgical aspects of available models for the study of various forms of liver disease. Furthermore, we summarize the translation of experimental liver surgery by highlighting surgical innovations, exploring key molecular mechanisms, and employing emerging treatment strategies.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4497-4508"},"PeriodicalIF":4.2,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11960460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764094","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":"Effect of Neutrophil Elastase Inhibitor (Sivelestat Sodium) on Oxygenation in Patients with Sepsis-Induced Acute Respiratory Distress Syndrome.","authors":"Tiejun Wu, Tao Wang, Jinjiao Jiang, Yue Tang, Lina Zhang, Zhiming Jiang, Fen Liu, Guiqing Kong, Tingfa Zhou, Ruijin Liu, Haipeng Guo, Jie Xiao, Wenqing Sun, Yuye Li, Yingying Zhu, Quan Liu, Weifeng Xie, Yan Qu, Xiaozhi Wang","doi":"10.2147/JIR.S506549","DOIUrl":"10.2147/JIR.S506549","url":null,"abstract":"<p><strong>Objective: </strong>Neutrophil elastase (NE) plays an important role in the development of acute respiratory distress syndrome (ARDS). Sivelestat sodium, as a selective NE inhibitor, may improve the outcomes of patients with sepsis-induced ARDS in previous studies, but there is a lack of solid evidence. This trial aimed to evaluate the effect of sivelestat sodium on oxygenation in patients with sepsis-induced ARDS.</p><p><strong>Methods: </strong>We conducted a multicenter, double-blind, randomized, placebo-controlled trial enrolling patients diagnosed with sepsis-induced ARDS admitted within 48 hours of the advent of symptoms. Patients were randomized in a 1:1 fashion to sivelestat or placebo. Trial drugs were administered as a 24-hour continuous intravenous infusion, for a minimum duration of 5 days and a maximum duration of 14 days. The primary outcome was the proportion of PaO₂/FiO₂ ratio improvement on Day 5 after randomization, defined by a greater than 50% improvement in PaO₂/FiO₂ compared with that on ICU admission or PaO₂/FiO₂ reached over 300 mmHg on Day 5.</p><p><strong>Results: </strong>The study was stopped midway due to a potential between-group difference in mortality observed during the interim analysis. Overall, a total of 70 patients were randomized, of whom 34 were assigned to receive sivelestat sodium and 36 placebo. On day 5, 19/34 (55.9%) patients in the sivelestat group had PaO₂/FiO₂ ratio improvement compared with 7/36 (19.4%) patients in the placebo group (risk difference, 0.36; 95% CI, 0.14 to 0.56, <i>p</i><0.001). The Kaplan-Meier curves showed a significantly improved 28-day survival rate in patients receiving sivelestat than those not (hazard ratio, 0.32; 95% CI, 0.11 to 0.95; <i>p</i>=0.041).</p><p><strong>Conclusion: </strong>In patients with sepsis-induced ARDS, sivelestat sodium could improve oxygenation within the first five days and may be associated with decreased 28-day mortality.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4449-4458"},"PeriodicalIF":4.2,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753080","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":"Platelet Factor 4: A Mysterious Chemokine in Inflammatory Regulation Diseases.","authors":"Yibing Ji, Qian Zhang, Hua Li, Lixia Chen, Yuzhuo Wu, Sheng Lin","doi":"10.2147/JIR.S504673","DOIUrl":"10.2147/JIR.S504673","url":null,"abstract":"<p><p>Platelet factor 4 (PF4), also referred to as CXCL4, is a significant component of the C-X-C chemokine family, predominantly localized within the alpha granules of platelets. It is recognized for its anti-heparin and anti-angiogenic properties. However, the involvement of PF4 in inflammatory processes has not been extensively investigated. This article aims to explore the diverse functions of PF4 in the context of inflammatory diseases, emphasizing its potential dual regulatory roles across various immune cell types and pathological conditions. Recent research has enhanced our comprehension of PF4, revealing its production not only in platelets but also in macrophages and activated T cells, thereby extending its functional repertoire beyond its conventional roles. Consequently, this review provides a thorough analysis of PF4's influence on inflammatory diseases and offers perspectives and recommendations for future research endeavors.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4481-4495"},"PeriodicalIF":4.2,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753083","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 the Systemic Inflammation Response Index and Severity of Acute Pancreatitis: A Retrospective Cohort Study.","authors":"Wen Wu, Yupei Zhang, Yilan Zhang, Xingguang Qu, Zhaohui Zhang, Rong Zhang","doi":"10.2147/JIR.S512553","DOIUrl":"10.2147/JIR.S512553","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to determine the association of the systemic inflammatory response index (SIRI) with severity in patients with acute pancreatitis (AP).</p><p><strong>Methods: </strong>This retrospective study was conducted using clinical data of 1514 patients with AP who were admitted between January 2019 and October 2023 to the First Clinical Medical College of Three Gorges University. SIRI was calculated as peripheral blood neutrophils × monocytes/lymphocytes ratio, and patients were divided into tertiles according to the SIRI levels. The comparison of demographic characteristics, clinical manifestations, laboratory parameters, and outcomes was made among groups. We also carried out multivariate logistic regression to analyze risk factors independently and forecast AP severity. Furthermore, the relationship between SIRI and AP severity was assessed using restricted cubic spline analysis. Subgroup analysis was conducted according to age, sex, body mass index, diabetes, white blood cell count, sequential organ failure assessment score, requirement for continuous renal replacement therapy, and etiology of AP.</p><p><strong>Results: </strong>Among the 1514 enrolled patients, 171 (11.3%) developed severe AP. Higher SIRI levels were independently related to the higher incidence of severe AP (adjusted P < 0.05) after adjusting the possible confounders. Nonlinear curve fitting demonstrated the reverse J-shaped relationship of SIRI with AP severity, with inflection points at 13. A consistent association was observed across various subgroup analyses.</p><p><strong>Conclusion: </strong>SIRI independently forecasts the severity of AP. This readily available biomarker may facilitate early stratification of risk and prompt intervention in clinical practice.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4471-4480"},"PeriodicalIF":4.2,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753073","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 Role of Neutrophil Extracellular Traps in Atherosclerosis: From the Molecular to the Clinical Level.","authors":"Yongfang Yuan, Changxin Sun, Xinyi Liu, Lanqing Hu, Zeping Wang, Xiaoya Li, Jingyi Zhang, Dexiu Li, Xiaonan Zhang, Min Wu, Longtao Liu","doi":"10.2147/JIR.S507330","DOIUrl":"10.2147/JIR.S507330","url":null,"abstract":"<p><p>Atherosclerosis is a chronic inflammatory condition that is typified by the deposition of lipids and the subsequent inflammation of medium and large arteries. Neutrophil extracellular traps (NETs) are fibrous meshworks of DNA, histones, and granzymes expelled by activated neutrophils in response to a variety of pathogenic conditions. In addition to their role in pathogen eradication, NETs have been demonstrated to play a pivotal role in the development of atherosclerosis. This article presents a review of the bidirectional interactions in which atherosclerosis-related risk factors stimulate the formation of NETs, which in turn support disease progression. This article emphasizes the involvement of NETs in the various stages of atherogenesis and development, influencing multiple factors such as the vascular endothelium, platelets, the inflammatory milieu, and lipid metabolism. The findings of this study offer new insights and avenues for further investigation into the processes underlying the formation and regulation of the vascular inflammatory microenvironment in atherosclerosis. Finally, potential targeted therapeutic strategies for NETs are discussed to facilitate their progression to clinical practice (Graphical Abstract).</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4421-4433"},"PeriodicalIF":4.2,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752818","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":"Distinct and Shared Molecular Mechanisms in Pediatric Antrochoanal Polyps and Chronic Rhinosinusitis with Nasal Polyps: A Proteomic and Metabolomic Integrative Analysis.","authors":"Yong-Chao Chen, Xin Wang, Yan-Wen Pan, Yi-Shu Teng, Hong-Guang Pan","doi":"10.2147/JIR.S507475","DOIUrl":"10.2147/JIR.S507475","url":null,"abstract":"<p><strong>Purpose: </strong>The underlying mechanisms of pediatric antrochoanal polyps (ACP)and chronic rhinosinusitis with nasal polyps (CRSwNP) remain largely unexplored. This study investigates their proteomic and metabolomic profiles to uncover unique and overlapping pathways, shedding light on their underlying causes.</p><p><strong>Methods: </strong>Specimens were collected from six children with ACP, six with CRSwNP, and six with normal inferior turbinate mucosa (CK) at Shenzhen Children's Hospital. Protein profiles were analyzed using data-independent acquisition (DIA) mass spectrometry, while metabolite profiles were assessed via non-targeted metabolomics (UPLC-MS/MS). Differences in proteins and metabolites were identified through statistical selection and bioinformatics, followed by integrated pathway analysis to explore their roles in disease processes.</p><p><strong>Results: </strong>Proteomic analysis identified 1000 differentially expressed proteins (DEPs) in ACP and 880 in CRSwNP compared to controls. Key DEPs in ACP included PEX1 and LYPD2, while CRSwNP included PEX1, CFAP52, SPAG6 and DHRS9. Metabolomic analysis identified 129 differential metabolites in ACP and 11 in CRSwNP, with 5-HTP showing opposite regulation between the two conditions. Pathway analysis pointed to oxidative stress and lipid metabolism disruptions in ACP, and immune and ciliary dysfunction in CRSwNP. Both conditions shared inflammation and extracellular matrix remodeling, but tryptophan metabolism diverged, with 5-HTP reduced in ACP and elevated in CRSwNP.</p><p><strong>Conclusion: </strong>This study highlights oxidative stress and lipid dysregulation as hallmarks of pediatric ACP, distinct from ciliary and immune dysfunction in CRSwNP, with inflammation and matrix remodeling as common features. The opposing regulation of 5-HTP reflects differences in tryptophan metabolism. Key molecules like PEX1, LYPD2, CFAP52, and 5-HTP emerge as potential biomarkers, offering promise for improved diagnosis and targeted therapies in nasal polyp-related conditions, but the small sample size and exploratory design require validation in larger cohorts to ensure clinical applicability.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4435-4447"},"PeriodicalIF":4.2,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753077","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":"Dysregulation of lncRNA GATA3-AS1 is Involved in the Pathogenesis of Pulpitis by the Regulation of miR-17-3p.","authors":"Leilei Li, Yumei Wang, Mingyan Hu","doi":"10.2147/JIR.S504048","DOIUrl":"10.2147/JIR.S504048","url":null,"abstract":"<p><strong>Purpose: </strong>When the pulp is inflamed or injured, cell morphology, gene expression, and synaptic connections change occur in the medullary dorsal horn, causing inflammation pain and formatting the pulpitis pain. To examine the impact of lncRNA GATA3-AS1 regulation of miR-17-3p on bioactivity and inflammation of lipopolysaccharides (LPS)-stimulated human dental pulp stem cells (hDPSCs).</p><p><strong>Patients and methods: </strong>The GATA3-AS1 expression in serum samples from patients with pulpitis, dental caries, and healthy control was examined using RT-qPCR. The GATA3-AS1 expression was verified using the GSE198359 dataset. hDPSCs were exposed to LPS to mimic in vitro pulpitis model. The viability and apoptotic rates of hDPSCs were determined by CCK-8 method and Flow cytometric analysis. The inflammatory cytokines levels were quantified using ELISA-based approach. A SOD assay kit was utilized to measure the activity of SOD. Bioinformatic analysis and dual-luciferase reporter assay were performed to explore the interaction between GATA3-AS1 and miR-17-3p, along with the potential mechanism.</p><p><strong>Results: </strong>Serum and tissue GATA3-AS1 levels were elevated in patients with pulpitis. Silencing GATA3-AS1 overturned the LPS stimulation inhibited viability and promoted apoptosis, inflammation, and oxidative stress in hDPSCs. GATA3-AS1 could target miR-17-3p, and miR-17-3p downregulation reversed silencing GATA3-AS1-mediated effects in LPS-induced hDPSCs. The GATA3-AS1-miR-17-3p axis might mediate the progression of pulpitis by many potential pathways, such as the PI3K-Akt signaling pathway and MAPK signaling pathway.</p><p><strong>Conclusion: </strong>GATA3-AS1 knockdown might have a protective effect on bioactivity, LPS-triggered inflammation, and damage in hDPSCs by regulating miR-17-3p, which might be a promising target for the treatment of pulpitis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4459-4469"},"PeriodicalIF":4.2,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753079","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":"Cerium Oxide-Loaded Exosomes Derived From Regulatory T Cells Ameliorate Inflammatory Bowel Disease by Scavenging Reactive Oxygen Species and Modulating the Inflammatory Response.","authors":"Simei Yue, Lingjiao Gong, Yulin Tan, Xiaodan Zhang, Fei Liao","doi":"10.2147/JIR.S502388","DOIUrl":"10.2147/JIR.S502388","url":null,"abstract":"<p><strong>Background: </strong>Abnormal immune homeostasis, which leads to the accumulation of reactive oxygen species (ROS) and an inflammatory response, plays a crucial role in accelerating the progression of inflammatory bowel disease (IBD). The lack of targeted therapeutic strategies significantly hampers the efficacy of clinical treatments for IBD. This study presents cerium oxide nanoparticle-loaded regulatory T cell-derived exosomes (exo@nCeO) as innovative anti-inflammatory and antioxidant agents specifically designed to address the effects of immune dysregulation.</p><p><strong>Methods: </strong>In this work, the morphology and antioxidant properties of nano-cerium oxide were characterized using transmission electron microscopy, as well as hydroxyl radical and 1,1-diphenyl-2-picrylhydrazyl radical assays. Tumor necrosis factor-α and dextran sulfate sodium were employed to establish cellular and animal models of IBD. The impact of exo@nCeO on ROS scavenging and anti-inflammatory activity in intestinal epithelial cells was assessed using dihydroethidium and 2,7-dichlorodihydrofluorescein staining, Western blotting, and apoptosis flow cytometry analysis. Hematoxylin and eosin staining, along with immunohistochemistry and immunofluorescence staining, were utilized to evaluate intestinal epithelial inflammation and ROS levels in the IBD mouse model.</p><p><strong>Results: </strong>The findings demonstrate that exo@nCeO possesses augmented anti-inflammatory properties and ROS scavenging abilities in intestinal epithelial cells. In murine models of IBD, exo@nCeO effectively maintained the integrity of the intestinal epithelial barrier and impeded the progression of IBD.</p><p><strong>Conclusion: </strong>This study introduces a novel therapeutic approach for IBD and underscores a potential strategy for addressing diseases associated with inflammation and oxidative stress.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"4395-4408"},"PeriodicalIF":4.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753075","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}