Inflammation最新文献

{"title":"Correction to: Nicorandil Regulates Ferroptosis and Mitigates Septic Cardiomyopathy via TLR4/SLC7A11 Signaling Pathway.","authors":"Jin-Shuai Lu, Jian-Hao Wang, Kun Han, Nan Li","doi":"10.1007/s10753-026-02625-0","DOIUrl":"10.1007/s10753-026-02625-0","url":null,"abstract":"","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":"49 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13668923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181036","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":"Fused Azine Derivatives Mitigate Long-Term Paracetamol-Induced Liver Fibrosis in Mice: Role of JNK1/ASK1 and Nrf2/HO-1 Signaling Pathways.","authors":"Ahmed Reda Shawky, Heba A Metwaly, Hanan M Ragab, Ahmed Wahid","doi":"10.1007/s10753-026-02579-3","DOIUrl":"10.1007/s10753-026-02579-3","url":null,"abstract":"<p><p>Liver fibrosis is a significant public health issue that necessitates an ongoing urge for efficient novel treatments. Our newly synthesized fused azine derivative compounds (1a, 1b, 2a, and 2b) were used in this study based on our promising results achieved by our team in previous studies on tacrine derivatives. This study investigated these compounds' hepatoprotective effect on mice with paracetamol (APAP) induced liver fibrosis and clarified their possible mechanisms. The administration of these compounds successfully reduced APAP-induced hepatic fibrosis through decreasing serum liver enzymes, as well as the hepatic pathological deterioration. Moreover, they increased hepatic antioxidants and countered oxidative stress caused by APAP. Furthermore, by lowering inflammatory cytokine levels and raising anti-inflammatory marker levels, these compounds effectively ameliorated the inflammatory response. Additionally, they decreased APAP induced levels of apoptosis-signal-regulating kinase-1 (ASK-1) and c-Jun-N-terminal kinase (JNK1). Additionally, they reduced caspase-3 and BCL2-associated X-protein (Bax) levels and promoted Nrf2 signaling pathway activation. Notably, the in-silico computer-assisted simulation docking results were consistent with the experimental measurements.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":"49 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989847","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":"Retraction Note: Chitotriosidase Expression during Monocyte-Derived Dendritic Cells Differentiation and Maturation.","authors":"Michelino Di Rosa, Daniele Tibullo, Daniela Cambria, Gisella Distefano, Salvatore Saccone, Francesco Di Raimondo, Lucia Malaguarnera","doi":"10.1007/s10753-026-02609-0","DOIUrl":"10.1007/s10753-026-02609-0","url":null,"abstract":"","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":"49 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919723","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":"Correction to: Identification of ATF3 as a Potential Key Biomarker for Hypertensive Nephropathy via Single-Cell Transcriptome Sequencing.","authors":"Fangyan Tan, Rong Hu, Jianlin Du, Ya Song","doi":"10.1007/s10753-026-02580-w","DOIUrl":"10.1007/s10753-026-02580-w","url":null,"abstract":"","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":"49 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13461647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706444","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":"Macrophage-derived FGF21 Restrains Endometritis By Suppressing Inflammation and Promoting Repair Through FGFR1.","authors":"Haiyan Liu, Zhuo Shi, Yihui Zheng, Xianliang Chen, Fatma Mrisho Haji, Weiwei Zhu, Feng Lin","doi":"10.1007/s10753-026-02537-z","DOIUrl":"10.1007/s10753-026-02537-z","url":null,"abstract":"<p><p>Endometritis is a prevalent inflammatory disorder that impairs female fertility, yet effective therapeutic strategies remain limited. Although the fibroblast growth factor (FGF) family has been increasingly implicated in inflammatory diseases, its role in endometritis remains largely unexplored. Here, systematic profiling of the FGF family identified FGF21 as the most significantly upregulated member in inflamed uterine tissues. Mechanistically, FGF21 is predominantly derived from macrophages and is positively associated with inflammatory activation. Functional studies showed that genetic deletion of FGF21 markedly exacerbates uterine inflammation, whereas exogenous administration of recombinant human FGF21 (rhFGF21) alleviates tissue injury and suppresses inflammatory responses in lipopolysaccharide-induced endometritis. At the cellular level, FGF21 attenuates macrophage-mediated inflammation and promotes proliferation while inhibiting cell death in endometrial stromal cells. Importantly, these protective effects are recapitulated in a clinically relevant methicillin-resistant Staphylococcus aureus-induced model, where rhFGF21 exhibits robust dose-dependent therapeutic efficacy. Mechanistically, FGF21 exerts its effects through activation of fibroblast growth factor receptor 1 (FGFR1), and pharmacological inhibition of FGFR1 abolishes its anti-inflammatory and pro-repair functions. Collectively, our findings identify macrophage-derived FGF21 as a critical regulator of endometrial inflammation and tissue repair, and highlight the rhFGF21 as a potential therapeutic drug for endometritis.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535844","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":"IL-17-associated Pro-inflammatory Programs in Aortic Valve Interstitial Cell Osteogenic Differentiation: JUN as a Candidate Regulator.","authors":"Yining Dai, Siyu Kong, Yupeng Yang, Yeshen Zhang, Yu He, Pengda He, Haobin Liu, Ning Tan, Pengcheng He, Ling Xue, Zhenyang Fu, Yuanhui Liu","doi":"10.1007/s10753-026-02565-9","DOIUrl":"10.1007/s10753-026-02565-9","url":null,"abstract":"<p><p>Calcific aortic valve disease (CAVD) involves fibro-calcific remodeling, in which osteogenic differentiation of valvular interstitial cells (VICs) is a key process. Although inflammation is implicated, uncertainties persist regarding how defined pro-inflammatory pathways are transcriptionally coupled to the VIC osteogenic program at the cell-intrinsic level. We implemented an interleukin-17 (IL-17) pathway-guided transcriptomic strategy in a pure human VIC osteogenic differentiation model. RNA sequencing identified osteogenesis-associated differentially expressed genes and IL-17-related inflammatory signatures. Functional enrichment and multilayer network analyses were applied to prioritize candidate regulatory nodes, followed by in vitro validation. An IL-17-associated transcriptional program was activated during VIC osteogenic differentiation and was enriched for stress-activated and MAPK-related inflammatory pathways. Network-based analyses consistently identified the AP-1 transcription factor JUN as a central regulatory node within this IL-17-linked signature. Experimentally, JUN expression increased during VIC osteogenic differentiation, and JUN silencing attenuated calcification. IL-17 A rapidly increased the p-c-JUN/JUN ratio, and prolonged treatment upregulated JUN and IL-17RA in a concentration-dependent manner. Exogenous IL-17 A stimulation enhanced calcification-related phenotypes in VICs, which were partially reversed by JUN knockdown. In a chronic kidney disease-induced mouse CAVD model, JNK inhibition with SP600125 reduced valve calcification and leaflet thickness. IL-17-associated inflammatory signaling is engaged during VIC osteogenic differentiation and may promote calcification, partially through a JUN-dependent mechanism. These findings provide insight into how inflammatory programs interface with osteogenic transcription and offer a framework for dissecting inflammation-driven calcification in CAVD.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535879","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 NLRP3/IL-6/EGR2/CSF-1 Axis Regulates Macrophage Differentiation and Inflammatory Resolution in Infection-Associated Wound Healing : NLRP3 Axis Controls Macrophage Fate in Wound Infection.","authors":"Jiao Kong, Hongjin Sheng, Mingxi Li, Zichao Wang, Haiyan Qin, Zhuoxia Wu, Lianbo Zhang","doi":"10.1007/s10753-026-02563-x","DOIUrl":"10.1007/s10753-026-02563-x","url":null,"abstract":"<p><p>Chronic Pseudomonas aeruginosa (P. aeruginosa) infection impairs wound healing, yet the underlying inflammatory mechanisms remain poorly understood. This study investigates how the NLRP3 inflammasome orchestrates macrophage differentiation and inflammatory resolution during infection-associated wound healing. A murine P. aeruginosa wound infection model was established. Macrophage polarization dynamics were assessed by flow cytometry (CD11b/F4/80/Arg1/iNOS/CD206/CD86) and histology. Wound healing outcomes were compared between wild-type and NLRP3-/- mice via closure kinetics, ECM analysis (Masson's trichrome/picrosirius red), and transcriptomic profiling. Mechanistic studies employed CRISPR-edited and pharmacologically modulated (MCC950/nigericin) THP-1/U937 cells, along with ChIP-qPCR, luciferase assays, and genetic rescue experiments. P. aeruginosa-infected wounds exhibited delayed healing, reduced ECM deposition, increased cellular senescence, and impaired fibroblast activation, with M1-dominant macrophage polarization and elevated NLRP3, ASC, caspase-1, IL-6, and IL-18. NLRP3-/- mice showed further delayed healing, decreased collagen I/III, reduced macrophage recruitment, and suppressed M1-to-M2 transition. Transcriptomics revealed downregulated Tlr4, Cd74, Egr2, and IL-6/JAK/STAT3 pathways. NLRP3 knockout impaired monocyte-to-macrophage differentiation (reduced CD14⁺ cells and adhesion), while NLRP3 overexpression enhanced it. EGR2 expression correlated with NLRP3 levels; EGR2 knockdown suppressed CSF-1/CSF1R and macrophage differentiation, whereas EGR2 overexpression rescued defects caused by NLRP3 knockout. Mechanistically, IL-6 promoted EGR2 nuclear translocation, and EGR2 directly bound the CSF-1 promoter to regulate its expression. The NLRP3 inflammasome drives macrophage differentiation and M1 polarization via the IL-6/EGR2/CSF-1 axis in infection-associated wound healing. Targeting this axis may represent a therapeutic strategy to modulate inflammatory responses and improve healing in infected wounds.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470417","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":"Propofol Inhibits Neutrophil Extracellular Traps Formation and Alleviates Sepsis-Induced Acute Lung Injury.","authors":"Wei Wang, Ran Xia, Chengmi Zhang, Muqiao Cheng, Yi Zheng, Haiying Ji, Fengying Xu, Shunan Lv, Nuo Xu, Yanfei Mao, Siyuan Li, Weiwei Li, Xueyin Shi","doi":"10.1007/s10753-026-02552-0","DOIUrl":"10.1007/s10753-026-02552-0","url":null,"abstract":"<p><strong>Background: </strong>Excessive neutrophil extracellular traps (NETs) formation contributes to lung tissue injury in sepsis-associated acute lung injury (ALI). Propofol, a commonly used sedative with anti-inflammatory and antioxidant properties, has been suggested to confer protection against ALI; however, its effects on NET sformation and the underlying mechanisms remain poorly defined.</p><p><strong>Methods and results: </strong>At the cellular level, we established an in vitro model of lipopolysaccharide (LPS)-induced NET formation using human peripheral blood neutrophils to evaluate the effects of propofol. Pharmacological inhibition experiments in vitro suggested that propofol may suppress NET release by modulating Akt/mTOR signaling, with a concomitant reduction in neutrophil autophagic activity. In parallel, we established an LPS-induced sepsis model in mice and administered propofol by intraperitoneal pretreatment. Lung histopathology and NET quantification showed that propofol treatment was associated with attenuated sepsis‑induced lung injury and suppressed NET formation in vivo. These protective effects were associated with increased Akt/mTOR pathway activity in lung tissue; however, because in vivo pathway blockade was not performed, the functional contribution of Akt/mTOR signaling to organ protection in this setting remains to be directly validated.</p><p><strong>Conclusions: </strong>Propofol attenuates sepsis-induced lung injury in association with suppressed NET formation. In vitro pharmacological inhibition experiments suggest that the Akt/mTOR axis may represent one pathway through which propofol suppresses NET release. However, direct in vivo validation of this mechanism (e.g., using pathway-specific inhibitors, conditional knockout models, or other loss-of-function approaches) remains necessary and should be addressed in future studies. Collectively, these findings identify a previously underappreciated mechanism of propofol action and support its potential adjunctive role in sepsis management.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470403","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":"GP130 Regulates Macrophage Polarization and Functional Recovery after Spinal Cord Injury in Rats: A Single-Cell RNA Sequencing Study.","authors":"Mengqi Gao, Danfen Zhang, Mingze Liu, Yezhong Wang, Yanbin Ke","doi":"10.1007/s10753-026-02564-w","DOIUrl":"10.1007/s10753-026-02564-w","url":null,"abstract":"<p><p>Neuroinflammation and macrophage polarization play important roles in secondary injury and functional recovery after spinal cord injury (SCI). GP130, the common signal-transducing receptor subunit of the IL-6 cytokine family, is closely associated with JAK/STAT3-mediated inflammatory signaling. However, its role in macrophage polarization after SCI remains unclear. This study investigated whether GP130 inhibition regulates macrophage polarization and improves functional recovery after SCI. A rat model of T10 spinal cord compression injury was established using a standardized microvascular clip compression method. The GP130 inhibitor SC144 was administered after SCI. Functional recovery was evaluated using BBB scoring and inclined plane tests. Histopathological, ultrastructural, immunofluorescence, flow cytometry, qRT-PCR, western blotting, ELISA, and single-cell RNA sequencing analyses were performed to evaluate tissue injury, inflammatory signaling, and macrophage polarization. Primary bone marrow-derived macrophages were further used to assess the direct effects of GP130 knockdown or pharmacological inhibition on macrophage phenotype in vitro. SCI induced severe locomotor impairment, tissue disruption, ultrastructural damage, and activation of GP130-related inflammatory signaling. SC144 treatment improved functional recovery, reduced inflammatory cytokine expression, and attenuated downstream STAT3 activation. Single-cell RNA sequencing revealed a prominent monocyte/macrophage-related myeloid-cell response after SCI and transcriptional heterogeneity within the myeloid compartment. Immunofluorescence and flow cytometry showed that GP130 inhibition reduced M1-like marker expression and promoted M2-like marker expression in vivo. In primary macrophages, GP130-siRNA and SC144 similarly suppressed M1-like pro-inflammatory marker expression and enhanced M2-like reparative marker expression. GP130 inhibition modulates macrophage polarization and promotes functional recovery after T10 spinal cord compression injury. These findings suggest that GP130-related inflammatory signaling may be a potential therapeutic target for regulating macrophage-mediated neuroinflammation after SCI.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445990","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":"Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.","authors":"Tianqi Wei, Xin Huang, Jing Zhu, Guanying Liu, Baiyi Zuo, Zhaokang Zhou, Beilei Xu, Lingling Luo, Chengrang Li","doi":"10.1007/s10753-026-02570-y","DOIUrl":"10.1007/s10753-026-02570-y","url":null,"abstract":"<p><p>Oxidative stress-mediated melanocyte injury and subsequent inflammation constitute essential pathogenic mechanisms underlying vitiligo. The secretion of diverse cytokines plays a crucial role in modifying the inflammatory environment characteristics of skin lesions. Interleukin 32 (IL32) is a multifunctional cytokine recognized for its potent pro-inflammatory effects. Here, we observed significantly enhanced IL32 expression in vitiligo skin lesions. The present study investigates the role of IL32 in oxidative stress-driven melanocyte inflammation and its contribution to vitiligo progression by establishing knockdown and overexpression models in PIG cell lines. Our findings demonstrate that oxidative stress triggers IL32 production in melanocytes, and increased IL32 exacerbates oxidative stress-mediated cellular injury. IL32 suppression activates the Nrf2 pathway and mitigates the oxidative stress response. Furthermore, transcriptomic analysis revealed that IL32 may promote the secretion of multiple inflammatory cytokines and chemokines in melanocytes in vitro, especially CXCL9, thereby facilitating the recruitment of CD8⁺ T cells. Notably, IL32 accelerates depigmentation in the mouse model of vitiligo. These results highlight the therapeutic promise of targeting IL32 to attenuate inflammation and oxidative damage in melanocytes associated with vitiligo.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445953","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}