Journal of Inflammation Research最新文献

{"title":"The Role of Inflammatory Biomarkers (IL-1, IL-6, TNF-α, and Alpha-Amylase) in Saliva on Post-Odontectomy Swelling: A Rapid Review.","authors":"Fauzah Iramawati Saim, Endang Sjamsudin, Nuroh Najmi","doi":"10.2147/JIR.S536809","DOIUrl":"10.2147/JIR.S536809","url":null,"abstract":"<p><strong>Background: </strong>Odontectomy is a commonly performed surgical procedure in the oral cavity and has several possible postoperative complications, including swelling. In addition to clinical examination, post-odontectomy swelling can be identified by utilizing saliva samples to analyze inflammatory biomarkers. The purpose of this study was to determine the role of inflammatory biomarkers IL-1, IL-6, TNF-α, and alpha-amylase in saliva on post-odontectomy swelling.</p><p><strong>Methods: </strong>A rapid literature review of clinical studies was conducted using the PRISMA framework. Article searches were performed on six databases (PubMed, ScienceDirect, SpringerLink, Cochrane Library, and EBSCOhost) using boolean operators and hand searching on Google Scholar.</p><p><strong>Results: </strong>Ten articles met the inclusion criteria. A risk of bias assessment was conducted using the JBI critical appraisal tools. Seven articles analyzed alpha-amylase, two articles analyzed TNF-α, and one article analyzed IL-1, IL-6, and TNF-α simultaneously to see the swelling or inflammation that occurs post-odontectomy. These four biomarkers were examined before, immediately after, or up to several days after the procedure. Significant elevations in biomarkers including IL-1, IL-6, TNF-a, and alpha-amylase are seen in the majority of articles. Post-procedure alpha-amylase elevation was observed along with swelling, pain, and fear associated with the odontectomy procedure. Increases in IL-1, IL-6, and TNF-α were observed due to tissue manipulation during the procedure that initiated the production of these proinflammatory cytokines.</p><p><strong>Conclusion: </strong>Inflammatory biomarkers IL-1, IL-6, TNF-α, and alpha-amylase in saliva play a role in post-odontectomy swelling, as their levels increase the intensity of swelling or inflammation also tends to rise. These biomarkers contribute to swelling through mechanisms involving immune cell recruitment, increased vascular permeability, and acute responses to pain and stress. Although it is constrained by the lack of relevant research, this review provides recommendations for further research into the most pertinent salivary biomarkers for identifying post-odontectomy swelling.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12227-12243"},"PeriodicalIF":4.1,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12417694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040288","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":"Xianglian Anchang Decoction Mitigates Ulcerative Colitis via Inhibition of TLR-4-Mediated Pyroptosis.","authors":"Shixiong Zhang, Yuhua Wang, Xuetong Ren, Haoyu Chen, Tianyu Gao, Yang Liu, Lishan Lu, Junzhuo Ma, Haiyan Bai, Yangang Wang","doi":"10.2147/JIR.S533936","DOIUrl":"10.2147/JIR.S533936","url":null,"abstract":"<p><strong>Background: </strong>Xianglian Anchang Decoction (XLAC) shows significant promise in treating ulcerative colitis (UC) based on clinical experience. However, the specific mechanism of XLAC treatment for UC is still not well understood.</p><p><strong>Purpose: </strong>This study aims to explore the pharmacological mechanism of XLAC in treating UC through network pharmacology and experimental verification.</p><p><strong>Methods: </strong>In this study, DSS-induced UC mouse model was established to evaluate the effects of XLAC on body weight, Disease Activity Index scores, spleen index, and colon length. Pathological change and intestinal barrier integrity were analyzed via hematoxylin-eosin, periodic acid-Schiff staining, immunofluorescence, RT-qPCR, Western blot, and ELISA. Network pharmacology and bioinformatics analyses were employed to predict potential targets of XLAC, followed by molecular docking to validate the binding affinity between key components and TLR4.</p><p><strong>Results: </strong>XLAC significantly ameliorated weight loss, colon shortening, and splenomegaly in UC mice (<i>P</i> < 0.001), restored intestinal barrier integrity, and increased the expression of tight junction proteins (ZO-1/Occludin) and goblet cell numbers. Network pharmacology identified TLR4 as a key target, and molecular docking demonstrated strong binding affinity (Vina score < -5) between XLAC active components (eg, trans-4-coumaric acid, methyl cinnamate) and TLR4. In vivo experiments confirmed that XLAC downregulated the protein levels of TLR4, NLRP3, and GSDMD-N, as well as the mRNA expression of IL-1β and IL-18 (<i>P</i> < 0.05), thereby suppressing pyroptosis.</p><p><strong>Conclusion: </strong>XLAC alleviates UC inflammation and intestinal barrier damage by targeting TLR4 to inhibit NLRP3 inflammasome activation and GSDMD-mediated pyroptosis. This study provides mechanistic insights into the clinical efficacy of XLAC for UC treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12245-12261"},"PeriodicalIF":4.1,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12417687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040319","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":"SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.","authors":"Farouk Baboni, Kingsley Miyanda Tembo, Xi Zhou, Qingwen Li, Chen Dai, Yuanyuan Zhao, Samiratou Batoko, Peixiang Lan, Zhishui Chen","doi":"10.2147/JIR.S534623","DOIUrl":"10.2147/JIR.S534623","url":null,"abstract":"<p><p>SET domain-containing lysine methyltransferase 7 (SETD7) is a critical enzyme that methylates lysine residues on both histone and non-histone proteins, thereby regulating gene expression and protein function. This methyltransferase plays a versatile and context-dependent role in a wide range of physiological processes, including cell differentiation, reactive oxygen species (ROS) signaling, oxidative stress regulation, and energy metabolism. SETD7's dual nature is highlighted by its paradoxical involvement in various diseases such as cancer, asthma, and Alzheimer's disease, where it can either promote or suppress pathological progression depending on the cellular environment and molecular context. The multifaceted functions of SETD7 underscore its importance in maintaining cellular homeostasis but also present significant challenges for therapeutic targeting. Although selective inhibitors like Cyproheptadine and (R)-PFI-2 have recently been identified, the development of highly specific and effective therapies remains complex due to SETD7's broad regulatory roles and the potential for unintended effects on normal physiological processes. These challenges necessitate nuanced therapeutic strategies, including the exploration of combination treatments and context-specific modulation to maximize efficacy while minimizing adverse outcomes. This review comprehensively explores SETD7's structure, subcellular localization, and diverse biological functions in both normal and disease states. By elucidating the dual and context-dependent nature of SETD7, it aims to provide a framework for future research focused on unraveling its molecular mechanisms and advancing targeted therapeutic approaches that leverage its unique regulatory capabilities.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12191-12225"},"PeriodicalIF":4.1,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12417711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040245","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":"CpG ODN Combined with Gold Nanorods Enhances Immune Activation and Its Potential Mechanism.","authors":"Shiwen Zhang, Changqiang Wang, Jing Jiang, Linlu Li, Jiaqi Luo, Jingying Zhu, Renxu Chen","doi":"10.2147/JIR.S528371","DOIUrl":"10.2147/JIR.S528371","url":null,"abstract":"<p><strong>Background: </strong>Immune escape of tumor cells is a common problem with tumor photothermal therapy utilizing gold nanorods (Au NRs). Whether CpG ODN, an immune adjuvant, can synergize with Au NRs to activate the immune response and its potential mechanism is not clear.</p><p><strong>Methods: </strong>The effect of Au NRs combined with CpG ODN (Au NRs-C) on the activity of various immune-related cells, such as double-positive T cells, macrophages, NK cells, Th17, and Treg. The expression levels of various immune and inflammation-related factors, such as IL-1R1, IL-6, IL-17, and TNF-α were characterized. Transcriptome sequencing analysis was used to explore the potential immunomodulatory mechanisms of Au NRs-C. Whether immune activation was enhanced by antibody-functionalized Au NR upon binding to CpG ODN was assessed.</p><p><strong>Results: </strong>Flow cytometry and ELISA analyses indicate that both Au NRs and CpG ODN increase pro-inflammatory cytokine levels and immune activation. However, Au NRs-C demonstrated superior immune activation potential. Furthermore, Au NRs stimulate the expression of Treg, while Au NRs-C significantly inhibit this effect. This suggests that the conjugation of CpG ODN with Au NRs not only greatly enhances the immune activation but also compensates for some of their deficiencies in eliciting immune responses. Transcriptome sequencing uncovered DEGs mainly localized to immune and pro-inflammatory cytokine pathways. PPI analysis identified six hub genes: <i>FOXM1, HMOX1, UBE2C, E2F1, PECAM1</i>, and <i>FCGR3A</i>. Moreover, CpG conjugation with antibody functionalization- Au NRs enhances immune stimulation.</p><p><strong>Conclusion: </strong>Au NRs-C promotes immune activation by eliciting changes in the activity of immune-associated cells and expression of inflammatory factors through multiple pathways, such as MHC antigen presentation and Toll-like receptor-mediated immune processes.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12089-12103"},"PeriodicalIF":4.1,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023438","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":"Integrated Single-Cell and Transcriptome Analysis with Experimental Validation Reveals PANoptosis-Related Gene Signatures in the Immune Microenvironment of Autoimmune Thyroiditis.","authors":"Zhuo Zhao, Ziyu Liu, Qun Wang, Hao Gao, Nan Song, Xiao Yang","doi":"10.2147/JIR.S525270","DOIUrl":"10.2147/JIR.S525270","url":null,"abstract":"<p><strong>Purpose: </strong>Autoimmune thyroiditis (AIT) is the most common organ-specific autoimmune disease, and its pathogenesis is closely related to the inflammatory microenvironment driven by immune cell penetration. The role of the newly proposed concept of PANoptosis in immune-related diseases is gradually being revealed. However, there is currently a lack of reports on PANoptosis in AIT. This study aims to clarify the relationship between PANoptosis gene, cell subgroup distribution, immune penetration, and AIT through a comprehensive analysis of scRNA-seq and bulk RNA-seq data combined with animal and clinical validation.</p><p><strong>Patients and methods: </strong>Initially, we integrated bulk RNA-seq and scRNA-seq data from AIT in public databases to identify immune cell subpopulations and the distribution and abundance of PANoptosis within them. Subsequently, we applied ssGSEA to assess the association between immune cell infiltration and inflammatory responses in AIT patients versus healthy individuals. Furthermore, we utilized the WGCNA tool to integrate PANoptosis genes with immune functions and screened for gene modules most significantly correlated with the immune-inflammatory effects of AIT. Finally, an animal model was established and clinical samples were collected for RT-qPCR, immunohistochemical staining,Enzyme-linked immunosorbent assay (ELISA) and ROC curve to predict the diagnostic value for further verification.</p><p><strong>Results: </strong>Through bioinformatics analysis, we identified 14 functionally heterogeneous cell subpopulations and 5 differentially expressed PANoptosis-related genes (AIM2, ZBP1, NLRP6, MLKL, and FAS). Experimental validation revealed that these differentially expressed genes were significantly upregulated in autoimmune thyroiditis (AIT). Moreover, they might promote the infiltration of inflammatory lymphocytes and the secretion of inflammatory cytokines in thyroid tissue through the PANoptosis pathway, with AIM2 potentially playing a central role.</p><p><strong>Conclusion: </strong>In summary, our study reveals the characteristics of the immune microenvironment of AIT and highlights the clinical potential of PANoptosis-Related genes (AIM2, ZBP1, NLRP6, MLKL, and FAS) as diagnostic biomarkers.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12123-12143"},"PeriodicalIF":4.1,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12415770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029811","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":"IRF6 Enhances IFN-β Expression and Inhibits Viral Replication to Reduce the Severity of Herpetic Stromal Keratitis.","authors":"Zhi Liu, Likun Xia","doi":"10.2147/JIR.S526580","DOIUrl":"10.2147/JIR.S526580","url":null,"abstract":"<p><strong>Purpose: </strong>Herpes simplex virus type 1 (HSV-1) infection of the human eye can lead to herpes simplex keratitis, which is the leading cause of infectious blindness worldwide. Inflammation invading the corneal stroma causes herpetic stromal keratitis (HSK). Interferon regulatory factor 6 (IRF6) is a member of the interferon regulatory factor family and is involved in the antiviral response against human papillomavirus 16. However, the mechanism related to the involvement of IRF6 in the host anti-HSV-1 response is unclear, and how latent infection and viral reactivation trigger corneal stromal inflammation remains unknown. Therefore, we investigated the role of IRF6 in HSV-1 infection.</p><p><strong>Methods: </strong>Proteomic detection techniques indicated that IRF6 was expressed at low levels in the corneas of HSK model mice. The antiviral effects of IRF6 have been demonstrated in animal and cellular studies. HSV-1 replication was activated when IRF6 was silenced in human corneal epithelial cells (HCECs), and IRF6 overexpression inhibited viral replication. HSK was established after locally inoculating mouse corneas with lentivirus to overexpress IRF6.</p><p><strong>Results: </strong>The degree of inflammation was attenuated, and proinflammatory cytokine secretion was reduced in the mice overexpressing IRF6 compared with that in the lentivirus control mice, suggesting that IRF6 attenuates the severity of HSK. Silencing of protein kinase C delta and receptor-interacting serine/threonine kinase 4 reduced IRF6 phosphorylation and inhibited its degradation during HCEC infection with HSV-1.</p><p><strong>Conclusion: </strong>These findings indicate that IRF6 is involved in the immune response against HSV-1 virus, and IRF6 can be used as a therapeutic target for treating HSK.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12045-12058"},"PeriodicalIF":4.1,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015577","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":"Combination of Polydatin and Hawthorn Leave Flavonoids Ameliorate Atherosclerotic Plaque Vulnerability in ApoE^-/- Mice by Regulating Ferroptosis via the Nrf2/HO-1/GPX4 Axis.","authors":"Jiye Chen, Xiaonan Zhang, Changxin Sun, Zeping Wang, Xiaoya Li, Lanqing Hu, Yongfang Yuan, Min Wu, Longtao Liu","doi":"10.2147/JIR.S530995","DOIUrl":"10.2147/JIR.S530995","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) is a chronic inflammatory vascular disease in which ferroptosis plays a crucial role. While the combination of polydatin (PD) and Hawthorn leaf flavonoids (HLF), termed PD and HLF combination (PH), is effective against AS, its impact on plaque vulnerability and the underlying mechanisms remain unclear.</p><p><strong>Methods: </strong>ApoE^-/- mice were fed a high-fat diet (HFD) for 12 weeks to establish an AS model and treated with PD, HLF and Simvastatin for 8 weeks. Histological characterization of atherosclerotic lesions was performed using pathological staining. Transmission electron microscopy (TEM) was used to evaluate mitochondrial damage. Lipid peroxidation levels were assessed using ELISA. Immunofluorescence staining was performed to verify Nrf2 nuclear translocation. Expression of the Nrf2/HO-1/GPX4 axis was detected using Western blotting and PCR.</p><p><strong>Results: </strong>HFD significantly promoted AS lesion formation and instability, and caused severe iron overload and lipid peroxidation in atherosclerotic lesions. PH significantly reduced dyslipidemia and suppressed atherosclerotic plaque progression in ApoE-/- mice. Meanwhile, the PH combination visibly reduced iron accumulation and improved mitochondrial ultrastructure. Additionally, PH combination decreased the levels of ROS, MDA, 4HNE, 8-OHdG, and Fe²⁺, while increasing GSH levels. Further studies showed that the PH combination enhanced the translocation of Nrf2 into the nucleus, HO-1, GPX4, SLC7A11, FPN1, and FTH1 expression, and inhibited cytoplasmic Nrf2 and TFR1 expression.</p><p><strong>Conclusion: </strong>PH combination reduced the instability of atherosclerotic lesions in ApoE^-/- mice by modulating iron metabolism and lipid peroxidation through activation of the Nrf2/ HO-1/GPX4 axis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12105-12121"},"PeriodicalIF":4.1,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12417686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040230","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":"Identification of Potential Targets for EGFR-Regulated Nucleus Pulposus Degeneration Using Single-Cell RNA Sequencing and Machine Learning.","authors":"Xiaoyao Peng, Yi Wang, Yangyang Chen, Yuxiang Hu, Fashuai Wu, Lu Zhang, Weihua Xu, Yulong Wei","doi":"10.2147/JIR.S530776","DOIUrl":"10.2147/JIR.S530776","url":null,"abstract":"<p><strong>Introduction: </strong>While nucleus pulposus cell (NPC) degeneration is a primary driver of intervertebral disc degeneration (IVDD), the cellular heterogeneity and molecular interactions underlying NPC degeneration remain poorly characterized. Previous studies have shown that EGFR signaling plays a significant role in NPC differentiation and collagen matrix production. Consequently, this study aims to identify the critical downstream regulatory molecule of EGFR in the process of NPC degeneration.</p><p><strong>Methods: </strong>We conducted subpopulation identification and functional analysis on scRNA-seq results in the GSE165722 dataset. Through pseudotime analysis, we identified genes with significant changes. Furthermore, we performed single-gene GSEA based on EGFR expression levels and conducted WGCNA to identify hub genes. Then, a combination of three machine learning algorithms (Lasso, XGBoost, and Random Forest), ROC curve, and validation in clinical specimens was employed to identify potential downstream regulatory molecule of EGFR associated with NPC degeneration. Finally, the regulatory effect of EGFR on potential downstream molecules was validated through both in vitro and in vivo experiments.</p><p><strong>Results: </strong>NPC from six severe IVDD samples were classified into six subpopulations, among which Fib-NPC was identified by functional and pseudotime analyses as a late-stage degenerative subpopulation linked to IVDD, with upregulated EGFR expression observed during degeneration. Five hub genes were identified through the intersection of pseudotime analysis, single-gene GSEA, and WGCNA. By integrating the results from three machine learning and validating through ROC curve and IHC, JAK1 was further identified as a downstream regulatory target of EGFR. Then, we found that JAK1 expression was elevated in NPC under oxidative stress, but remained unchanged following Gefitinib pretreatment. We further developed an IVDD model using mice with NP-specific inactivation of EGFR, which demonstrated that EGFR inactivation attenuated the upregulation of JAK1 in the degenerated NP region.</p><p><strong>Conclusion: </strong>This study reveals a significant degenerative process in NPC and indicates that EGFR may contribute to this degeneration by regulating JAK1, thereby identifying a potential therapeutic target for delaying IVDD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12059-12075"},"PeriodicalIF":4.1,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12415117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029809","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":"Investigation into the Therapeutic Efficacy and Inflammatory Modulatory Effects of the Combined Use of 0.01% Atropine Eye Drops and Orthokeratology Lenses in the Management of Myopia Among Adolescent Patients.","authors":"Hui Wang, Junfeng Piao, Geunchang Yoo, Danqi Li, Jun Liu, Jeon In-Chul","doi":"10.2147/JIR.S539831","DOIUrl":"10.2147/JIR.S539831","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the therapeutic efficacy and inflammatory modulatory effects of combined 0.01% atropine eye drops and orthokeratology (OK) lenses in controlling myopia progression among adolescent patients.</p><p><strong>Methods: </strong>This retrospective study analyzed clinical data from 90 adolescent patients (90 eyes) with myopia treated from April 2021 to June 2023. Patients were divided into two groups: control group (n=45, treated with OK lenses alone) and observation group (n=45, treated with OK lenses combined with 0.01% atropine). Baseline and 1-year post-treatment measurements included refractive status, axial length (AL), corneal parameters, ocular surface indices, tear film stability, endothelial cell morphology, inflammatory cytokine levels in tears, and incidence of adverse events.</p><p><strong>Results: </strong>After 1 year, both groups showed myopic progression, but the observation group exhibited significantly less axial elongation (0.12 ± 0.08 mm vs 0.21 ± 0.09 mm; p < 0.001) and smaller increases in refractive error (p < 0.001). Corneal curvature and central corneal thickness were also significantly lower in the observation group (p < 0.05). The pupil diameter increased more in the observation group (p = 0.002), consistent with atropine's pharmacologic effect. Ocular surface damage was less severe, with lower OSDI (p = 0.002) and staining scores (p < 0.001). Tear film stability was better preserved, as reflected by higher NIBUT and TBUT values (p < 0.05). No significant differences in endothelial cell density or hexagonality were observed (p > 0.6). Tear cytokine levels (IL-1β, IL-6, TNF-α) increased in both groups but were significantly lower in the observation group (all p < 0.01). The incidence of adverse reactions was low and comparable between groups (p = 0.235), with no severe events reported.</p><p><strong>Conclusion: </strong>The combination of 0.01% atropine eye drops with orthokeratology lenses is more effective than orthokeratology alone in controlling myopia progression and mitigating ocular surface inflammation in adolescents, without increasing adverse effects.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"12077-12087"},"PeriodicalIF":4.1,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015572","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 Dual Role of Myokines in Fatigue Associated with Inflammatory Joint Diseases.","authors":"Grzegorz Chmielewski, Jakub Kuna, Łukasz Jaśkiewicz, Michalina Knapik, Mateusz Mikiewicz, Michał S Majewski, Magdalena Krajewska-Włodarczyk","doi":"10.2147/JIR.S545914","DOIUrl":"10.2147/JIR.S545914","url":null,"abstract":"<p><p>Fatigue is a prevalent and debilitating symptom in rheumatic diseases such as rheumatoid arthritis and psoriatic arthritis. Despite advances in reducing inflammation through treatments, fatigue often persists, underscoring its multifactorial etiology. A possible link between the persistent inflammation observed in rheumatic diseases and the onset of fatigue has been suggested. The discovery that skeletal muscles also secrete cytokines and myokines, has opened new avenues for research. This narrative review explores current mechanistic insights and evidence on the dural role of myokines in exacerbating or alleviating fatigue, particularly in the context of physical activity and chronic inflammation. Key myokines such as interleukin-6 (IL-6), myostatin, interleukin-15 (IL-15), brain-derived neurotrophic factor (BDNF), and irisin are examined for their influence on muscle-brain communication, neuroinflammation, and systemic metabolic processes. The findings highlight the potential of targeted myokine modulation as a therapeutic strategy for fatigue management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"11999-12020"},"PeriodicalIF":4.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12412675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015545","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}