Journal of Inflammation Research最新文献

{"title":"The Role of Type 2 Innate Lymphoid Cells in Adenoid Hypertrophy with Allergic Rhinitis Among Children and Related Potential Therapeutic Targets.","authors":"Yan Hao, Tian-Yong Hu, Mei-Zhen Zhao, Xian-Hai Zeng, Ke Li, Bao-Hui Cheng, Da-Bo Liu","doi":"10.2147/JIR.S515707","DOIUrl":"10.2147/JIR.S515707","url":null,"abstract":"<p><strong>Objective: </strong>Innate lymphoid cells (ILC) are a heterogeneous group of immune cells implicated in immune diseases. However, their specific roles in adenoid hypertrophy (AH), AH with allergic rhinitis (AH+AR), and AH with otitis media with effusion (AH+OME) remain poorly understood. This study aimed to characterize ILC subsets and their association with immunological profiles in these conditions.</p><p><strong>Methods: </strong>Flow cytometry was used to quantify ILC subsets in adenoid tissues from patients with AH, AH+AR, or AH+OME, and correlations between ILC subsets and clinical, immunological (serum and tissue cytokines), and histopathological parameters were further assessed.</p><p><strong>Results: </strong>ST2 mRNA and protein expression were significantly higher in AH+AR than in AH and AH+OME (p < 0.05). Serum IL-33 was elevated in AH+AR compared to AH (p = 0.0127), while IFN-γ was higher in AH than in AH+AR (p = 0.0044). IL-4 levels were higher in AH and AH+AR than in AH+OME (p < 0.005). Flow cytometry showed that ILC2 predominated in AH+AR (p = 0.0009 vs AH+OME), with higher ILC2/ILC1 and ILC2/ILC3 ratios in AH and AH+AR compared to AH+OME (p < 0.05). Correlation analysis indicated that ILC2 in AH+AR positively correlated with serum IgE, IL-4, IL-33, thymic stromal lymphopoietin (TSLP), and tissue IL-4, IL-33, TSLP, and IL-25 (p < 0.05). ILC3 inversely correlated with peripheral blood eosinophils (p = 0.0125) and positively with serum and tissue IL-17A (p < 0.05).</p><p><strong>Conclusion: </strong>ILC2 cells are significantly enriched in adenoid tissues of patients with AH+AR, with elevated ST2 and IL-33 levels supporting the activation of the IL-33/ST2/ILC2 signaling pathway. Targeting this pathway may offer novel therapeutic strategies for AH combined with allergic rhinitis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8593-8605"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12228517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575645","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 Factors Influencing Resorption of Herniated Part of Lumbar Disc Herniation: Comprehensive Review.","authors":"Qilong Lai, Guanyi Gong, Yukai Lu, Peijie You, Yicheng Zhu, Zhiqiang Wang, Shun Lin, Hong Jiang, Xiaochun Li, Jintao Liu","doi":"10.2147/JIR.S525233","DOIUrl":"10.2147/JIR.S525233","url":null,"abstract":"<p><strong>Abstract: </strong>This review systematically examines the mechanisms underlying the spontaneous resorption of lumbar disc herniation (LDH), focusing on vascularization, autophagy, apoptosis, macrophage activity, and the therapeutic potential of traditional Chinese medicine (TCM). We emphasize that resorption is influenced by factors such as herniation type, disease duration, and imaging biomarkers (eg, the bull's-eye sign). Additionally, this review summarizes recent progress in the study of resorption mechanisms following lumbar disc herniation, providing a reference for future clinical research.</p><p><strong>Methods: </strong>Literature was systematically searched in PubMed, Web of Science, and CNKI (2000-2024) using keywords: 'lumbar disc herniation,' 'resorption,' 'autophagy,' 'TCM.' Inclusion criteria: (1) human/animal studies; (2) MRI-confirmed LDH; (3) English/Chinese full texts. Exclusion criteria: case reports (n<10).</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8553-8562"},"PeriodicalIF":4.2,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575642","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":"Reduced Thioredoxin Regulates IL-1β Secretion via NLRP3 of IL-1β+ Alveolar Macrophages in COPD.","authors":"Lueli Wang, Rui Shi, Zhaoliang Li, Ruoqiu Ma, Chongyu Wang, Changli Xu, Rong Guo, Chuang Xiao, Xiaohua Du, Weimin Yang","doi":"10.2147/JIR.S513004","DOIUrl":"10.2147/JIR.S513004","url":null,"abstract":"<p><strong>Objective: </strong>Chronic obstructive pulmonary disease (COPD) is a disease with a complex etiology. The secretion of inflammatory factors, such as IL-1β and oxidative stress, plays an important role in the pathogenesis of COPD. The aim of this paper is to investigate the changes in the redox protein thioredoxin (TRX) in COPD and the role TRX plays in IL-1β release.</p><p><strong>Methods: </strong>We analyzed data from single-cell RNA sequencing (scRNA-seq) of COPD lung tissue in the GEO database. Changes in TRX expression levels and activity were assessed by protein activity analysis of alveolar macrophages(AM). Using Monocle2 and molecular dynamics(MD) to analyze which pathways through TRX achieves regulation of the inflammatory response. The analytical results were subsequently validated by constructing vivo and vitro models.</p><p><strong>Results: </strong>AM that specifically synthesize IL-1β were identified by scRNA-seq. No change in TRX expression levels and decreased protein antioxidant activity in IL-1β+ AM with COPD. We confirmed an increase in oxidized TRX (oxTRX) and a decrease in reduced TRX (reTRX) in COPD mouse model and THP-1 cell model. The decrease in reTRX was accompanied by the upregulation of NLRP3 activity, which played a catalytic role in the synthesis of IL-1β in this subgroup. This was subsequently confirmed in a cigarette smoke-induced THP-1 cell model. A decrease in reTRX level accompanied by an upregulation of NLRP3 activity, which plays a facilitating role in the synthesis of IL-1β. We determined that reTRX reduction was followed by depolymerization of thioredoxin-interacting protein (TXNIP) through MD and immune co-precipitation (CO-IP). Then TNXIP interacted with NLRP3 and up-regulate NLRP3 activity, which in turn promoted IL-1β release.</p><p><strong>Conclusion: </strong>Our study shows that the reTRX is abnormally altered in COPD and leads to the upregulation of NLRP3 activity in AM to enhance IL-1β production.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8563-8578"},"PeriodicalIF":4.2,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12227320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575643","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 Relationship Between Immune-Inflammatory Indexes and the Severity of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia: A Cross-Sectional Study at a Tertiary Hospital in China.","authors":"Yifan Wu, Jiayi Sheng, Xinwei Liu, Yongneng Huang, Yuwei Zhang, Ninghan Feng","doi":"10.2147/JIR.S523193","DOIUrl":"10.2147/JIR.S523193","url":null,"abstract":"<p><strong>Purpose: </strong>Lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH) are common urogenital system diseases in elderly men and can cause serious complications when the disease progresses to moderate and severe stages. Early and accurate identification is of great significance for prevention, treatment, and prognosis assessment. However, there is still a lack of effective and simple predictive indicators. This study aims to investigate whether immune-inflammatory markers derived from complete blood count (CBC) exhibit an independent association with the severity of BPH/LUTS.</p><p><strong>Patients and methods: </strong>This study included a total of 698 BPH/LUTS patients who met the inclusion criteria at the Department of Urology, Jiangnan University Medical Center. According to the International Prostate Symptom Score (IPSS) score, patients were divided into a mild group and a moderate-to-severe group. Binary logistic regression analysis was used to explore the association between the severity of BPH/LUTS and the neutrophil-to-lymphocyte ratio (NLR), systemic inflammatory response index (SIRI), and systemic immune-inflammatory index (SII).</p><p><strong>Results: </strong>The median age of the participants was 70.00 (65.00, 75.00) years. After adjusting for confounding factors, the NLR, SIRI, and SII were positively correlated with the severity of BPH/LUTS. Compared with the lowest quartile, the highest quartile of NLR (OR = 6.20 [3.49-11.02]), SIRI (OR = 7.49 [4.15-13.50]), and SII (OR =7.85 [4.73-16.61]) were most significantly associated with the risk of BPH/LUTS aggravation. In subgroups stratified by age, diet, physical activity, cardiovascular disease, and diabetes, NLR, SIRI, and SII were positively correlated with BPH/LUTS severity. In subgroups defined by waist circumference and dyslipidemia, SIRI and SII were positively correlated with BPH/LUTS severity. In the smoking subgroup, only SIRI showed a positive correlation with BPH/LUTS severity.</p><p><strong>Conclusion: </strong>The findings suggest that NLR, SIRI, and SII are affordable and readily available detection methods that can be used as indicators for assessing the severity of BPH/LUTS.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8509-8523"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540509","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":"Comment on \"Predictive Value of Advanced Lung Cancer Inflammation Index and Development of a Nomogram for Prognosis in Patients with Cervical Cancer Treated with Radiotherapy\" [Letter].","authors":"Kailang Li","doi":"10.2147/JIR.S542961","DOIUrl":"10.2147/JIR.S542961","url":null,"abstract":"","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8525-8526"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540505","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":"Host Immune Response to <i>Mycobacterium tuberculosis</i> Infection: Implications for Vaccine Development.","authors":"Qianfei Liu, Songnian Que, Yixuan Qiu, Mingxing Tang, Shaohua Liu, Guanteng Yang, Yuxiang Wang, Ang Deng, Xiaojiang Hu, Xuehui Lian, Qile Gao","doi":"10.2147/JIR.S517034","DOIUrl":"10.2147/JIR.S517034","url":null,"abstract":"<p><p>Tuberculosis (TB) is an infectious disease caused by <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) infection, including pulmonary tuberculosis and extrapulmonary tuberculosis. About a quarter of the people in the world are infected with TB, but only 5-10% of them will progress to active TB, posing a major challenge to the eradication of TB. The study of the host immune response to <i>Mtb</i> infection is a key aspect of the development of effective vaccines and immunotherapies to eradicate tuberculosis. In this review, we delve into the overview of animal models of TB infection and the host's innate and adaptive immune responses to <i>Mtb</i> infection. We discuss how <i>Mtb</i> is recognized and phagocytosed by macrophages, how it evades immune responses, the recruitment and mobilization of neutrophils and monocytes, the role of natural killer cells during the infection process, how dendritic cells initiate adaptive immunity, the important roles of CD4⁺ T cells and their subtypes in TB infection, how CD8⁺ T cells exert cytotoxic functions, and how B cells produce antibodies and exhibit memory characteristics to eliminate pathogens. Furthermore, we review the tuberculosis vaccines currently entering clinical trials, emphasizing that studying the host's immune responses following <i>Mtb</i> infection is crucial for the development of more effective vaccines, providing a theoretical foundation and direction for the treatment of tuberculosis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8429-8445"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540507","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":"IFNα/JAK/STAT1 Axis-Induced FBXO4 Modulates Muscle Cell Differentiation via β-Catenin Degradation in Dermatomyositis.","authors":"Liguo Yin, Hanbo Yang, Min Fu, Yanyan Bai, Naiwen Hu, Hongsheng Sun","doi":"10.2147/JIR.S506056","DOIUrl":"10.2147/JIR.S506056","url":null,"abstract":"<p><strong>Purpose: </strong>Dermatomyositis (DM) is an inflammatory myopathy characterized by chronic muscle inflammation and damage. Although the pathogenesis of DM has been widely reported to be related to chronic inflammation, the role of ubiquitin E3 ligases in DM remains unclear. In the current study, we aimed to investigate the biological roles of ubiquitin E3 ligase in DM.</p><p><strong>Methods: </strong>Deseq2 was used to screen the differential express genes in DM public datasets. Quantitative real time PCR and Western blot were used to examine the mRNA and protein levels. Co-immunoprecipitation assays were used to investigate the protein interactions between proteins. Dual-luciferase reporter assays were applied to investigate the regulation between transcription factors and targets.</p><p><strong>Results: </strong>In the current study, we screened public DM-related datasets and focused on ubiquitin-proteasome-related enzymes. Ultimately, we identified the ubiquitin E3 ligase FBXO4. FBXO4 was significantly upregulated in DM muscle tissues compared to normal controls. In human muscle cells (LHCN-M2), FBXO4 knockout led to significant upregulation of genes related to muscle cell differentiation and significant downregulation of genes enriched in cell cycle pathways, as revealed by RNA-seq. These results suggest that FBXO4 knockout promotes muscle cell differentiation. Mechanistic studies showed that FBXO4 ubiquitinates and degrades β-catenin, thereby inhibiting the Wnt/β-catenin signaling pathway and suppressing muscle cell differentiation. On the other hand, FBXO4 may promote muscle cell apoptosis in DM by degrading MCL1. Additionally, we found that FBXO4 is regulated by the IFNα/JAK/STAT1 signaling pathway in DM and identified FBXO4 as a direct target of STAT1.</p><p><strong>Conclusion: </strong>In conclusion, our findings suggest that IFNα/JAK/STAT1 signaling pathway elevates the expression of FBXO4 in DM and then it contributes to muscle atrophy by inhibiting differentiation and promoting apoptosis. Targeting FBXO4 may offer a novel therapeutic approach for DM.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8527-8539"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540508","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":"Decrease of Resolvin D1 and E1 in Patients with Chronic Epilepsy, Implicating Dysfunction of Neuroinflammation Resolution.","authors":"Hanli Li, Zhong Dong, Yujing Yang, Qibing Sun, Fengqing Lu, Ran Li, Weifeng Zhou, Wei Gui, Rupan Gao, Yu Wang","doi":"10.2147/JIR.S521679","DOIUrl":"10.2147/JIR.S521679","url":null,"abstract":"<p><strong>Objective: </strong>Inflammation resolution is mediated by specialized pro-resolving lipid mediators (SPMs). It's of high interest to understand the alterations of SPMs in chronic epilepsy.</p><p><strong>Methods: </strong>Sixty-five patients with chronic epilepsy, 43 healthy controls and 43 patients with non-inflammatory neurological disorders were enrolled in this study. Plasma and cerebrospinal fluid (CSF) levels of SPMs were measured using liquid chromatography-tandem mass spectrometry (LC-MS-MS). Moreover, Resolvin D1 (RvD1) and resolvin E1 (RvE1), as well as pro-inflammatory factors were analyzed by enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>LC-MS-MS found several lipid mediators were altered, especially plasma (<i>P</i> = 0.014) and CSF (<i>P</i> = 0.010) RvE1 levels were decreased in patients with chronic epilepsy. Furthermore, ELISA results showed that in plasma and CSF, RvD1 and RvE1 levels were both lower in patients with chronic epilepsy, while pro-inflammatory factors were higher than in controls. Moreover, plasma RvE1 level was independently negatively associated with the National Hospital Seizure Severity Scale scores (Β = -0.00636, <i>P <</i> 0.001). While plasma RvD1 level was correlated with Mini-Mental State Examination scores (R = 0.284, <i>P</i> = 0.022).</p><p><strong>Conclusion: </strong>This study demonstrated decreased levels of RvD1 and RvE1 both in plasma and CSF in patients with chronic epilepsy, suggesting impaired resolution of inflammation in chronic epilepsy. Targeting RvD1 and RvE1 may be a novel direction worthy of further research in the treatment of chronic epilepsy.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8541-8551"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540506","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":"Mild Chronic Colitis Exacerbates Intracerebral Inflammation in Mice with Parkinson's Disease Through LRRK2-Mediated Regulation of NF-κB Activation and Inhibition of Nrf2.","authors":"Manqi Yang, Linping Ke, Yiman Geng, Piao Hu, Yao Qiu, Ziwen Liu, Xueqin Zhang, Fuxin Wan, Joe Antony Jacob, Jingling Liao","doi":"10.2147/JIR.S526777","DOIUrl":"10.2147/JIR.S526777","url":null,"abstract":"<p><strong>Background and objective: </strong>Inflammatory bowel disease (IBD) is a known risk factor for Parkinson's disease (PD). Leucine-rich repeat kinase 2 (LRRK2), a protein associated with both disease, regulates inflammation in the colon and brain. However, the precise mechanism by which LRRK2 mediates the crosstalk between intestinal inflammation and PD neuropathology remains unclear. This study aims to elucidate how LRRK2 mediates the inflammatory response in both the gut and brain.</p><p><strong>Methods: </strong>A dual-hit (DSS+MPTP) mouse model was established to induce IBD and PD, along with separate single DSS-induced colitis and MPTP-induced PD models. LRRK2 expression was analyzed in the colon and striatum. Intestinal barrier integrity (ZO-1, Occludin), dopaminergic neuron loss and inflammation (TH, Iba-1 staining in SNpc/striatum), NF-κB and Nrf2 pathways activity, and levels of inflammatory cytokines (TNF-α, IL1-β, IL-6 and IL-10) in the colon and striatum was assessed.</p><p><strong>Results: </strong>In the colon, LRRK2 expression was significantly increased in all experimental groups compared to the control, with the highest levels observed in the dual-hit group. The elevated LRRK2 expression correlated with the reduction in ZO-1 and Occludin levels and an increase in inflammatory cytokines IL1-β and TNF-α. A similar pattern of LRRK2 expression was observed in the brain. The dual-hit group exhibited increased Iba-1 expression and a significant loss of dopaminergic neurons. Furthermore, the upregulation of LRRK2 was associated with NF-κB activation and Nrf2 inhibition in the brain.</p><p><strong>Conclusion: </strong>Mild chronic colitis induced by DSS may exacerbate brain inflammation in MPTP-induced PD mice by upregulating LRRK2 expression, leading to NF-κB activation and Nrf2 inhibition. We propose that LRRK2 may play a regulatory role in the NF- κB/Nrf2 interplay in PD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8493-8507"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553704","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":"Qimai Feiluoping Decoction Inhibits EndMT to Alleviate Pulmonary Fibrosis by Reducing PI3K/AKT/mTOR Pathway-Mediated the Restoration of Autophagy.","authors":"Jing Ma, Lu Ding, Xiaoyu Zang, Yingying Yang, Wei Zhang, Xiangyan Li, Daqing Zhao, Zepeng Zhang, Zeyu Wang, Linhua Zhao, Xiaolin Tong","doi":"10.2147/JIR.S515286","DOIUrl":"10.2147/JIR.S515286","url":null,"abstract":"<p><strong>Purpose: </strong>Pulmonary Fibrosis (PF) is a severe interstitial lung disease currently lacking effective prevention strategies. Endothelial mesenchymal transition (EndMT), a novel mechanism for fibroblast production, is closely associated with PF. The precise mechanisms underlying the contribution of EndMT-derived fibroblasts to PF, however, remain unclear.</p><p><strong>Methods: </strong>Using network pharmacology, molecular docking, and molecular dynamics, we identified the key targets and pathways through which Qimai Feiluoping decoction (QM) combats PF. EndMT and autophagy proteins were quantified in bleomycin (BLM) -induced C57BL/6 mice, human umbilical vein endothelial cells (HUVECs), and zebrafish using Western blotting (WB), quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC), immunofluorescence (IF), Transwell migration assays, and transmission electron microscopy (TEM), revealing the targets and pathways through which QM mitigates PF.</p><p><strong>Results: </strong>Network pharmacology, molecular docking, and molecular dynamics suggest that QM combats PF by modulating the PI3K/AKT/mTOR pathway. Observations from the study indicated that QM was found to alleviate EndMT by restoring autophagy, primarily through inhibition of the PI3K/AKT/mTOR signaling pathway in both BLM-induced C57 mice and HUVECs. Supporting evidence from zebrafish models demonstrated that QM not only counteracts EndMT but also improves a range of vascular functional disorders and remodeling issues following EndMT.</p><p><strong>Conclusion: </strong>Our research validates the active compounds, core targets, and signaling pathways through which QM counters PF, providing valuable insights for its therapeutic application in PF management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8447-8475"},"PeriodicalIF":4.2,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528296","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}