Inflammation Research最新文献

{"title":"GSDMD deficiency mitigates intestinal damage via macrophage pyroptosis control in experimental NEC.","authors":"Yihang Yang, Xinyi Yang, Yue Ma, Xinli Liu, Dandan Mo, Cuilian Ye, Qin Deng, Wenli Han, Xionghui Ding, Chunbao Guo","doi":"10.1007/s00011-025-02062-z","DOIUrl":"10.1007/s00011-025-02062-z","url":null,"abstract":"<p><p>Necrotizing enterocolitis (NEC) is primarily associated with an intensified inflammatory response within macrophage inflammasomes. This increased activity initiates pyroptotic cell death in macrophages, a process meticulously regulated by the protein gasdermin D (GSDMD). The precise role of macrophage pyroptosis in NEC is yet to be comprehensively understood. Our research explores the critical role of GSDMD in macrophage pyroptosis during experimental NEC. We have discovered a significant correlation between GSDMD and macrophage pyroptosis in the terminal ileum of infants afflicted with NEC. By utilizing GSDMD-deficient models and disulfiram, a compound that disrupts GSDMD-mediated pore formation, we observed a significant alleviation of NEC symptoms in mouse pups, along with a reduced presence of intestinal macrophages. Furthermore, bone marrow-derived macrophages (BMDMs) from GSDMD-deficient mice showed a decrease in overall macrophage numbers and a shift away from M1 polarization. Interestingly, although GSDMD inhibition bolstered the antibacterial capabilities of macrophages, their phagocytic activity towards zymosan particles remained unchanged. In summary, our findings underscore the essential function of GSDMD in regulating macrophage inflammasome responses and suggest that GSDMD could serve as a potential therapeutic target for NEC.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"110"},"PeriodicalIF":5.4,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144872930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prominent fibroblast growth factor 21 with less abundant tumor-associated macrophages in hepatic mass of the conditional mgmt-deleted mice using LysM-Cre system.","authors":"Supistha Sontidejkul, Pornpimol Phuengmaung, Wilasinee Saisorn, Warerat Kaewduangduen, Kent Doi, Atsadang Boonmee, Salisa Benjaskulluecha, Tanapat Palaga, Asada Leelahavanichkul","doi":"10.1007/s00011-025-02077-6","DOIUrl":"https://doi.org/10.1007/s00011-025-02077-6","url":null,"abstract":"<p><strong>Background: </strong>Fibroblast growth factor 21 is a molecule responsible for cell energy regulation, mainly produced from hepatocytes, while O6-methylguanine-DNA methyltransferase is a mandatory enzyme for DNA repair.</p><p><strong>Methods: </strong>Because tumors in the livers might enhance hepatocytic FGF-21 production for supporting tumor-associated macrophages (TAM) to promote cancers, the intrahepatic tumor injection model was performed.</p><p><strong>Results: </strong>Indeed, intrahepatic injection of MC38 cells in wild-type mice increased FGF-21 in serum and liver tissue. Murine hepatocytes excreted FGF-21 after induction by cell stresses, lipopolysaccharide, and MC38 supernatant, while human hepatocytes (HepG2) produced FGF-21 after incubation with the conditioned media of CaCO₂, but neither HK2 nor H292. Intrahepatic MC38 injection in mgmt null mice demonstrated a lower tumor size and intratumoral TAM (CD206-positive cells) but higher FGF-21 production when compared with intrahepatic tumors in mgmt control. Additionally, MC38 supernatant induced M2-like polarization, which was enhanced by recombinant FGF-21. Furthermore, TAM induction by MC38 supernatant caused cell stresses only in mgmt null macrophages but not in mgmt control cells, as indicated by increased cell-free DNA and malondialdehyde with reduced maximal respiration. The TAM transformation-induced cell injury was neutralized by recombinant FGF-21.</p><p><strong>Conclusion: </strong>TAM transformation in mgmt null macrophages induced more severe cell injuries than mgmt control macrophages, leading to the less abundant intratumoral TAM and increased FGF-21 to attenuate the injuries in mgmt null mice with tumors. Further studies on FGF-21 and MGMT in cancers are interesting.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"109"},"PeriodicalIF":5.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired endothelial cell-derived CX3CL1-mediated macrophage efferocytosis in hypertrophic cardiomyopathy based on multi-omics analysis.","authors":"Yan Zhang, Xin Yan, Xiao-Lei Fu, Hai-Bing Yang, Yi-Min Yan, He-Fan He, Li Yang","doi":"10.1007/s00011-025-02075-8","DOIUrl":"https://doi.org/10.1007/s00011-025-02075-8","url":null,"abstract":"<p><strong>Background: </strong>Clinical studies have demonstrated that multiple inflammatory related proteins are associated with hypertrophic cardiomyopathy (HCM). However, the precise role of these factors in the pathogenesis of HCM remains uncertain.</p><p><strong>Methods: </strong>The link between inflammatory related proteins and HCM was analyzed using Mendelian randomization (MR), followed by bioinformatics to explore the role of inflammatory related proteins in HCM. In vivo and in vitro models of HCM were established to elucidate how inflammatory related proteins influence HCM progression.</p><p><strong>Results: </strong>Our MR analysis revealed a negative correlation between the inflammation related protein CX3CL1 and HCM. Bioinformatics and in vivo data similarly demonstrated a reduction in CX3CL1 expression in HCM. CX3CL1 was found to be mainly expressed in cardiomyocytes and endothelial cells via the Human Protein Atlas database and its' expression in both cells was obviously downregulated after being treated by angiotensin-II. Importantly, functional characteristics and correlation analysis of CX3CL1 indicated that it was most closely associated with macrophages efferocytosis. Consequently, we examined the signature molecules (AXL, MERTK, and TYRO3) associated with efferocytosis, which revealed a significant decrease in their expression in HCM. Notably, recombinant mouse CX3CL1 (rm-CX3CL1) reversed this process.</p><p><strong>Conclusions: </strong>In conclusion, CX3CL1-meidated impaired efferocytosis plays a critical role in the initiation and development of HCM, and modulation of CX3CL1 may prove advantageous in managing HCM progression.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"108"},"PeriodicalIF":5.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strain-specific responses to dextran sulfate sodium-induced ulcerative colitis in BALB/c and C57BL/6 mice: Comparative analysis of local versus extra-intestinal manifestations.","authors":"Priyanka Tiwari, Gopabandhu Jena","doi":"10.1007/s00011-025-02072-x","DOIUrl":"https://doi.org/10.1007/s00011-025-02072-x","url":null,"abstract":"<p><strong>Objective and design: </strong>Dextran sulfate sodium (DSS)-induced colitis in rodents is considered a well-established experimental model for the induction of ulcerative colitis (UC) and its extra-intestinal manifestations (EIMs). The influence of strain on EIMs of UC remains poorly understood. The present study elucidated the strain-specific responses to different concentrations of DSS and its effects on the local (colon), systemic (DNA damage in peripheral blood), and extra-intestinal (liver, pancreas, brain) manifestations.</p><p><strong>Methods: </strong>BALB/c and C57BL/6 mice, two commonly used rodent strains, were assigned to control and DSS (0.5%, 1%, 2%, and 3% w/v) treatment groups. DSS was provided in drinking water for 7 days over three cycles, with a 7-day inter-cycle remission. No other treatments or interventions were provided.</p><p><strong>Results: </strong>BALB/c exhibited gradual weight loss even at the lower doses of DSS, while C57BL/6 showed an early and sustained weight loss, particularly at the higher doses, contributing to greater severity and mortality. C57BL/6 exhibited significant systemic and colonic damage, with elevated inflammatory markers (nitrite, TNF-α, IL-1β, LPS) and reduced IL-10 in all the target organs. In contrast, MPO activity and goblet cell loss were more significant in BALB/c. C57BL/6 exhibited significant increase in the intestinal permeability as well as expression of TLR4 in colon and brain as compared to BALB/c mice. Overall, C57BL/6 mice showed significant increase in UC associated brain damage at higher concentrations of DSS, whereas BALB/c exhibited significant liver and pancreatic damage in a dose-dependent manner to DSS exposure. The expression of apoptotic cells and NF-κB/ICAM-1 increased dose-dependently in both the strains, with distinct patterns of expressions at the target organs.</p><p><strong>Conclusion: </strong>Strain-specific differences in inflammation, cell adhesion, apoptosis, and systemic DNA damage may be responsible for the differential severity, susceptibility, and the extent of colonic and extra-colonic damage observed in BALB/c and C57BL/6 mice. These findings underscore the importance of selecting an appropriate experimental model for UC and can offer translational relevance in predicting organ susceptibility and managing the intestinal and extraintestinal complications.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"107"},"PeriodicalIF":5.4,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IFNGR1, IRF8 genetic polymorphisms modulate the susceptibility of non-tuberculous mycobacteria pulmonary disease and influence the patients' treatment outcomes and immune status.","authors":"Li-Ping Cheng, Zhi-Bin Liu, Lei Wang, Jie Cao, Qing-Rong Qu, Hai Lou, Xiao-Na Shen, Juan Yang, Yuanyuan Yu, Rui Juan Zheng, Wei Sha, Qin Sun","doi":"10.1007/s00011-025-02071-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02071-y","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the association of genetic polymorphisms in MB21D1 (Mab-21 domain-containing 1), TMEM173 (Transmembrane Protein 173), IFNB1 (Interferon beta 1), IFNGR1 (Interferon gamma receptor 1), IFNGR2 (Interferon gamma receptor 2), IRF3 (Interferon Regulatory Factor 3), and IRF8 (Interferon Regulatory Factor 8) with susceptibility to non-tuberculous mycobacteria pulmonary disease (NTM-PD) as well as their correlation with the treatment outcomes and immune status of patients.</p><p><strong>Methods: </strong>Forty-four tagSNPs from the candidate genes were genotyped in a 2-phase cohort study including an initial discovery phase involving 707 NTM-PD patients and 726 healthy controls and a replication phase involving 357 NTM-PD patients and 400 controls. The frequencies and distributions of genotypes were compared between the case and control groups. Treatment success rates, sputum culture conversion rates, imaging characteristics, and peripheral blood immunological indices were compared among patients with different genotypes.</p><p><strong>Results: </strong>Individuals with the IFNGR1 rs2234711 A/A genotype were more susceptible to MAC-PD compared to those with the G/G genotype (discovery phase OR = 1.752, P.adj = 0.025; replication phase OR = 2.143, P.adj = 0.019). Patients with the rs2234711 A/A genotype exhibited significantly lower treatment success rates and sputum culture conversion rates, along with elevated levels of peripheral blood heparin-binding protein (HBP), erythrocyte sedimentation rate, and interleukin-10, but significantly decreased interleukin-1β levels (all P < 0.05). Individuals with the IRF8 rs2280378 A/A genotype were more susceptible to MAB-PD (discovery phase OR = 2.302, P.adj = 0.014; replication phase OR = 2.465, P.adj = 0.015). Compared to G/G genotype patients, those with the rs2280378 A/A genotype exhibited lower treatment success rates and sputum culture conversion rates, were more likely to develop pulmonary cavities and multiple lung field involvement, and showed elevated levels of peripheral blood HBP and C-reactive protein, along with significantly reduced levels of serum interleukin-12 P70, tumor necrosis factor-α, and CD8 + T lymphocytes (all P < 0.05).</p><p><strong>Conclusion: </strong>In the Chinese Han population, IFNGR1 genetic polymorphisms are closely associated with MAC-PD susceptibility, while IRF8 genetic polymorphisms are associated with MAB-PD susceptibility. Variants in IFNGR1 and IRF8 significantly affect the immune status and treatment outcomes of MAC-PD and MAB-PD patients, respectively.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"106"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfidptosis-related genes RPN1 inhibits the progression of hepatocellular carcinoma by regulating cell cycle, may be a new therapeutic targets.","authors":"Rongzheng Zhang, Kun Zhou, Meng Wu, Han Qiao, Le Yu, Xi Jin, Jingbo Li, Guanglu Dong, Shuyun Zhang","doi":"10.1007/s00011-025-02070-z","DOIUrl":"10.1007/s00011-025-02070-z","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is the predominant type of liver cancer with a poor prognosis. Treatment methods include surgery, ablation, liver transplantation, and immunotherapy. Programmed cell death (PCD) plays a significant role in the occurrence and treatment of HCC, and disulfidoptosis, as a novel type of PCD, is associated with tumor prognosis and anti-tumor immunity. The purpose of this study is to explore the role and molecular mechanisms of disulfidoptosis-related genes (DRGs) in the occurrence and development of HCC.</p><p><strong>Methods: </strong>We developed an HCC prognostic signature comprising three DRGs: RPN1, SLC7A11, and GYS1, using the TCGA database. The mRNA expression levels of the signature genes in peripheral blood mononuclear cells (PBMCs) of 196 patients were detected by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR), and the expression of RPN1 in 23 pairs of HCC tissues and adjacent non-tumor tissues were validated by RT-qPCR and immunohistochemistry (IHC). Additionally, the role of RPN1 in HCC was investigated through EdU Assay, CCK8 Assay, wound Healing Test, transwell experiments. The changes of cell cycle were detected by flow cytometry, and the changes of Cyclin (CDK1, CDK2, Cyclin D1, Cyclin E1) were detected by Western blot. We carried out in vivo experiments in a BALB/c nude mice model of HCC established through subcutaneous injection.</p><p><strong>Results: </strong>RPN1 was significantly upregulated in paired HCC tissues (p < 0.001). HCC group was also significantly higher in PBMCs than healthy group (p < 0.001). Interestingly, RPN1 expression were higher in the HBV group and HBV-LC group than in HBV-HCC group (p < 0.001). IHC experiments confirmed that RPN1 was also up-regulated in HCC tissues (p < 0.05). In vitro experiments showed that knockdown of RPN1 promoted the proliferation and migration of HCC cells, while overexpression of RPN1 inhibited these functions. Flow cytometry and Western blot confirmed that knockdown of RPN1 in HCCLM3 and Huh7 cells resulted in a decrease in the proportion of G0/G1 phase cells and an increase in the proportion of G2/M phase cells. Meanwhile, the expression levels of cell cycle proteins (CDK1, CDK2, Cyclin D1, and Cyclin E1) were significantly elevated. In vivo, overexpression of RPN1 in Hep3B cells can inhibit tumor growth.</p><p><strong>Conclusions: </strong>In vitro and in vivo experiments confirmed that the overexpression of RPN1 can significantly suppresses the progression of HCC by regulating the cell cycle. RPN1 could potentially serve as a new therapeutic target for HCC.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"105"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanosensitive ion channels and inflammation: key links in cellular signal transduction.","authors":"Shanmei Du, Kui Liu","doi":"10.1007/s00011-025-02057-w","DOIUrl":"https://doi.org/10.1007/s00011-025-02057-w","url":null,"abstract":"<p><p>Inflammation is a crucial pathological process in many diseases. Mechanosensitive ion channels, like the Piezo family and TRPV4, play a significant role in the inflammatory response. They sense mechanical stimuli and convert them into intracellular signals, regulating physiological processes. During inflammation, their activation is linked to inflammatory signal transduction. By modulating intracellular calcium levels and activating pathways such as NF-κB and MAPK, these channels promote the release of inflammatory factors, which exacerbate the inflammatory response. These ion channels are involved in the pathogenesis of various inflammatory-related diseases, including cardiovascular, respiratory, digestive, and neurological disorders. Animal and cell experiments, such as gene manipulation and drug intervention, have been used to explore their relationship with inflammation. Targeting these channels shows therapeutic potential, but the safety and efficacy of such treatments need to be evaluated. In summary, mechanosensitive ion channels are important research targets in inflammation. Although further study is required to fully understand their mechanisms and therapeutic applications, they hold promise for treating inflammatory diseases.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"104"},"PeriodicalIF":4.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Annexin A1 is crucial during Toxoplasma gondii infection promoting the modulation of inflammation and intestinal and central nervous system barrier functions.","authors":"Rayane Aparecida Nonato Rabelo, Rafaela das Dores Pereira, Natalia Fernanda de Melo Oliveira, Samuel Luiz Teixeira Porto, César Luís Nascimento Barbosa, Livia Fernanda Dias Santana, Fernando Bento Rodrigues Oliveira, Mayra Fernanda Ricci, Celso Martins Queiroz-Junior, Cínthia Firmo Teixeira, Vivian Barbosa Santos Alvarenga, Luiza Pinheiro Silva, Viviani Mendes de Almeida, Lirlândia Pires Sousa, Angelica Thomaz Vieira, Mauro Martins Teixeira, Caio Tavares Fagundes, Fabiana Simão Machado","doi":"10.1007/s00011-025-02065-w","DOIUrl":"https://doi.org/10.1007/s00011-025-02065-w","url":null,"abstract":"<p><strong>Background: </strong>Toxoplasmosis promotes acute and chronic symptoms ranging from ocular to severe congenital or neurotoxoplasmosis. A proper host immune response and a healthy gut microbiota control the pathophysiology of toxoplasmosis, presenting an opportunity for pro-resolving mediators.</p><p><strong>Objective: </strong>Here, we evaluated the role of the anti-inflammatory/pro-resolving protein annexin (Anx)A1 in Toxoplasma gondii (Tg) infection.</p><p><strong>Results: </strong>AnxA1 levels increase in the brain during Tg infection, and AnxA1 knockout (KO) mice display higher susceptibility to disease, an increased number of brain cysts, an inflammatory response, severe lesions, and brain permeability, along with lower claudin-5 and occludin expression. Notably, AnxA1 deficiency increased the number of IBA-1⁺ cells in the brain, macrophages/neutrophils/dendritic cells producing IL-10 and TNF, and Th2 and CD8 T cells producing IL-17 compared to wild-type cells. An increased number of Tregs and innate cells producing TNF has been observed in the spleen. Moreover, the absence of AnxA1 increases gut inflammation, alters microbiota composition, reduces mucus production, increases intestinal permeability, and promotes bacterial translocation from the gut to the liver. Furthermore, imipenem treatment restored animal survival, prevented bacterial translocation into the liver, and reduced brain inflammation. = CONCLUSION: Collectively, our data demonstrate that AnxA1 is critical for regulating the pathogenesis of Tg infection and unveils a possible therapeutic target for this disease.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"103"},"PeriodicalIF":4.8,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the intersection of atherosclerosis and Alzheimer's disease: the role of inflammation and complement activation.","authors":"Emilia Vataja, Giorgio Ratti, Adrian Safa, Marta Pagano, Luigia Ferrante, Seppo Meri, Karita Haapasalo","doi":"10.1007/s00011-025-02069-6","DOIUrl":"10.1007/s00011-025-02069-6","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) and Alzheimer's disease (AD) are both multifactorial in nature and share many risk factors. Vascular dementia and AD may occur together, and a substantial proportion of AD cases also have signs of cardiovascular disease, a relationship well-established by cohort studies. The risk factors could contribute to persistent smoldering inflammation, including activation of complement at sites of endothelial injury and/or by accumulation of molecular aggregates.</p><p><strong>Methods: </strong>To examine the possible bridging points between AD and AS, we constructed a comprehensive narrative review.</p><p><strong>Results: </strong>A connecting point between AD and AS is inflammation. Contrary to prior assumptions, a significant linkage exists between systemic inflammation and neuroinflammation. Activities of complement, a key effector of innate immunity, are of special interest in the pathogenesis of both diseases.</p><p><strong>Conclusion: </strong>AS and AD share a partially overlapping array of pathophysiological mechanisms.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"102"},"PeriodicalIF":4.8,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibulin-7 and its bioactive fragments: emerging immunomodulatory roles in disease.","authors":"Saloni Gupta, Puneet Kumar, Pranita P Sarangi","doi":"10.1007/s00011-025-02067-8","DOIUrl":"https://doi.org/10.1007/s00011-025-02067-8","url":null,"abstract":"<p><strong>Background: </strong>Fibulins belong to the family of secreted glycoproteins regulating several cellular processes. Fibulin7 (Fbln7) is one of its recent members, and it was first identified in the developing tooth. Fbln7 is also expressed in specialized tissues such as cartilage, eye, and the placenta. Previous reports have suggested that its C-terminal (Fbln7-C) fragment and not the full-length protein can inhibit angiogenesis, and modulate systemic inflammation and cancer.</p><p><strong>Method: </strong>We have performed a literature review based on published original and review articles that encompass the significant effect of Fbln7 and its bioactive fragments on immune cell functions from central databases, including PubMed and Google Scholar.</p><p><strong>Results and conclusion: </strong>Recent reports have also shown that several shorter peptides of Fbln7-C, such as FC-10, regulate innate immune cell functionality and have anti-angiogenic properties. Since the discovery of Fbln7, many research groups have improved our understanding of the role of Fbln7, Fbln7-C, and short peptides in immunoregulation and pathophysiology of many disease conditions, such as sepsis, kidney injury, and different cancers (e.g., murine breast tumors and glioblastoma). This review will present an updated overview of the research findings on the immunomodulatory, anti-angiogenic, and other regulatory properties of Fbln7 and its fragments, which will provide further insight into its significance, mode of action, and possible implications for future research and therapeutics.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"101"},"PeriodicalIF":4.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}