Frontiers in Immunology最新文献

{"title":"IKZF1 exacerbates the inflammatory response by epigenetically modulating mitochondrial function following acute peritonitis.","authors":"Guanya Liu, Pengfei Hu, Ying Dong, Yamin Xu, Zhengyao Yang, Zihao Qi, Yuantao Su","doi":"10.3389/fimmu.2025.1600903","DOIUrl":"10.3389/fimmu.2025.1600903","url":null,"abstract":"<p><strong>Background: </strong>Macrophages play pivotal roles in immune homeostasis and host defense against pathogens, yet their excessive activation can lead to tissue damage. Acute peritonitis induced by cecal ligation and puncture (CLP) is associated with dysregulated macrophage-mediated inflammation. IKZF1, a transcription factor, has been implicated in immune regulation, but its role in CLP-induced macrophage activation remains unclear. This study aimed to investigate the molecular mechanism of IKZF1 in regulating inflammatory responses during acute peritonitis.</p><p><strong>Method: </strong>Using a murine CLP-induced peritonitis model, we analyzed IKZF1 expression in macrophages via RT-qPCR and western blot. Lenalidomide (Len), an IKZF1 inhibitor, was administered to assess its effects on macrophage inflammation and lung injury. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS), ATP levels, and succinate accumulation. Mechanistic studies included chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and HDAC3 activity assays. SDHB expression and acetylation status were analyzed under LPS stimulation, with acetate supplementation used to modulate histone H3K9 acetylation.</p><p><strong>Results: </strong>IKZF1 expression was significantly upregulated in macrophages during CLP-induced peritonitis. Len treatment suppressed IKZF1, attenuating inflammatory responses and mitigating lung injury. Mechanistically, IKZF1 directly repressed SDHB expression by recruiting HDAC3 to deacetylate SDHB, leading to mitochondrial dysfunction and amplified inflammation. Supplementation with acetate restored H3K9ac levels at the SDHB promoter, counteracting LPS-induced suppression of SDHB. These findings highlight an IKZF1/HDAC3-SDHB-succinate axis driving macrophage hyperactivation.</p><p><strong>Conclusion: </strong>IKZF1 exacerbates macrophage inflammation in CLP-induced peritonitis by epigenetically silencing SDHB via HDAC3-mediated deacetylation, thereby disrupting mitochondrial metabolism and amplifying pro-inflammatory signals. Targeting IKZF1 or enhancing acetylation may represent novel therapeutic strategies for acute inflammatory conditions. This study establishes IKZF1 as a potential biomarker and therapeutic target for mitigating excessive inflammation in peritonitis.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1600903"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185786","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":"Proteomics of plasma-derived extracellular vesicles from human patients identifies biomarkers for monitoring visceral leishmaniasis therapy.","authors":"Ana Torres, Ana Montero-Calle, Marina Lozano-Rendal, Carmen Sánchez, Lorena Bernardo, Jose Carlos Solana, Juan Victor San Martin, Rodrigo Barderas, Javier Moreno, Eugenia Carrillo","doi":"10.3389/fimmu.2025.1646335","DOIUrl":"10.3389/fimmu.2025.1646335","url":null,"abstract":"<p><strong>Introduction: </strong>The most severe form of leishmaniasis, visceral leishmaniasis (VL), lacks standardized validated early predictors of treatment success or relapse. To distinguish between active infection and successful treatment, we searched for protein biomarkers in plasma-derived extracellular vesicles (EVs).</p><p><strong>Methods: </strong>The proteomic profiles of EVs from immunocompetent patients with active VL (n=12) or 1, 3, or 6 months after completing a standard treatment regimen (n=12 each) were analyzed by LC-MS/MS. Six candidate biomarkers were further tested by ELISA in whole plasma.</p><p><strong>Results: </strong>132 human proteins were differentially expressed in active VL- versus successfully treated patients. Pathway analysis identified pathogenic mechanisms associated with VL and pathways related to effective cure. SAA is directly measurable in whole plasma and exhibits differential expression levels, emerging as a promising, easily measurable, non-specific prognostic biomarker for patient management. Remarkably, we also identified <i>Leishmania</i> spp. proteins in EV samples, indicating a new source of parasite biomarkers in human samples.</p><p><strong>Conclusion: </strong>Plasma EVs contain protein biomarkers that can be used to monitor the response to treatment, some of which are detectable in whole plasma after 1 month of treatment. Our study also provides a proteomic landscape of plasma EVs involved in VL, offering insight into the pathogenesis of this complex disease.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1646335"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185523","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":"Age-enhanced MAGIC algorithm predicts mortality in pediatric aGVHD: a multicenter study.","authors":"Na Song, Hao Xiong, Ri Xu, Wen-Geng Cheng, Shan He, Shaoyang Deng, Benshan Zhang, Dao Wang","doi":"10.3389/fimmu.2025.1660861","DOIUrl":"10.3389/fimmu.2025.1660861","url":null,"abstract":"<p><strong>Introduction: </strong>Acute graft-versus-host disease (aGVHD) is a major contributor to non-relapse mortality (NRM) in pediatric patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT). Although the MAGIC algorithm has been validated in adults, its predictive value in children remains insufficiently explored.</p><p><strong>Methods: </strong>We conducted a prospective multicenter cohort study including 105 Chinese pediatric allo-HSCT recipients diagnosed with aGVHD between May 2019 and August 2023. Endpoints were 6-month NRM, overall survival (OS), and Day-28 treatment response. Multivariable analyses incorporated clinical variables together with the Panel 2 score, hereafter referred to as Panel 2,using Cox regression for NRM/OS and logistic regression for treatment response.</p><p><strong>Results: </strong>Age ≥12 years (hazard ratio 4.36, 95% CI 1.62-11.75; P=0.003) and a high Panel 2 score (HR 3.09, 95% CI 1.08-8.82; P=0.035) were independent predictors of 6-month NRM and OS. The high-risk (HR) group, defined by the combination of age ≥12 years and a high Panel 2 score, had markedly higher NRM than the low-risk (LR) group (71% vs 12.2%; HR 5.00, 95% CI 1.75-9.56; P=0.001) and significantly worse OS (P<0.001). Panel 2 was also predictive of Day-28 treatment response, with lower CR/PR rates in the high versus low group (62% vs 92%; P<0.001).</p><p><strong>Discussion: </strong>The Panel 2 score effectively predicted NRM, OS, and treatment response in pediatric aGVHD. Incorporating age ≥12 years further enhanced risk stratification, enabling clear separation between HR and LR groups. These findings support the potential clinical utility of this combined model and warrant validation in larger, international pediatric cohorts.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1660861"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185610","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":"Telitacicept as a novel B cell-targeted therapy in autoimmune encephalitis: a case report.","authors":"Zhishan Jiang, Huafeng Liang, Sheng Chen, Qinming Zhou","doi":"10.3389/fimmu.2025.1640790","DOIUrl":"10.3389/fimmu.2025.1640790","url":null,"abstract":"<p><p>Autoimmune encephalitis (AE) comprises immune-mediated neuroinflammatory disorders presenting diverse neuropsychiatric symptoms and antibody-specific manifestations. Despite standard immunotherapy, residual disability, treatment intolerance, and relapse risks highlight unmet clinical needs. Telitacicept, a dual target fusion protein that inhibits B-lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL), suppresses pathogenic B cell activation and autoantibody production, presenting a mechanism-driven therapeutic potential for AE management. Three AE cases with distinct therapeutic complexities are detailed in our study: (1) An anti-N-methyl-D-aspartate receptor (NMDAR) antibody-positive patient experienced recurrent relapses and was a comorbid individual with upper gastrointestinal bleeding. (2) An anti-leucine-rich glioma inactivated 1 (LGI1) antibody patient resisted corticosteroids, intravenous immunoglobulin, and ofatumumab treatment. (3) A newly diagnosed, anti-LGI1 antibody and anti-contactin-associated protein 2 (CASPR2) antibody dual-positive patient required sequential therapy to consolidate the remission and facilitate prednisone tapering. Telitacicept administration achieved symptom remission across all cases, accompanied by reduced antibody titers and stable outcomes over six months. Our case series evaluates the use of telitacicept in AE patients with varied antibody subtypes, particularly for patients with relapsed or refractory disease, intolerance to CD20-targeted agents, or steroid-related complications. Moreover, telitacicept may serve as an effective sequential therapy to sustain remission and reduce long-term steroid dependency.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1640790"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185702","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: Tumor-restricted activation of Vγ9Vδ2 T cells via bispecific Evobodies: a novel strategy for safe and potent immunotherapy in ovarian cancer.","authors":"Hans-Heinrich Oberg, Malte Deseke, Steffen Krohn, Dorothee Winterberg, Matthias Peipp, Dirk Bauerschlag, Klaus-Peter Künkele, Daniela Wesch, Christoph Baumann","doi":"10.3389/fimmu.2025.1672018","DOIUrl":"https://doi.org/10.3389/fimmu.2025.1672018","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fimmu.2025.1628501.].</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1672018"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185650","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":"Editorial: Cellular and molecular regulators in non-neoplastic immune-mediated diseases.","authors":"Noha M Elemam, Iman M Talaat, Omar A El Meligy, Jennifer E Hundt","doi":"10.3389/fimmu.2025.1694308","DOIUrl":"https://doi.org/10.3389/fimmu.2025.1694308","url":null,"abstract":"","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1694308"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185744","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 immunomodulatory and antitumor properties of the bacterial metalloprotease Oligopeptidase A are mediated by TLR4/MyD88/TRIF and MAPK signaling pathways.","authors":"Priscila Silva, Gabrielli Novaes Silva, Filipe Menegatti Melo, Carolina de Amat Herbozo, Tarciso Almeida Sellani, Samanta Lopes Tomaz, Amanda Campelo L De Melo, Larissa Reis Da Silva, Rodrigo Berzaghi, Marcelo F M Marcondes, Fellipe Bronze, Thaysa Paschoalin, Isaias Glezer, Adriana K Carmona, Felipe Valença Pereira, Elaine Guadelupe Rodrigues","doi":"10.3389/fimmu.2025.1630886","DOIUrl":"10.3389/fimmu.2025.1630886","url":null,"abstract":"<p><strong>Introduction: </strong>Immunosuppressive factors within the tumor microenvironment hinder effective antitumor immune responses and limit the efficacy of current immunotherapies. Immunomodulators offer an alternative by activating immune effectors. Proteases from various sources used as cancer therapy adjuvants have shown promise in inhibiting tumor growth. Our previous work showed that the bacterial metalloprotease arazyme has a strong in vivo antimetastatic effect in the B16F10-Nex2 murine melanoma model. Interestingly, heat-inactivated arazyme also exhibited antitumor properties dependent on an intact adaptive immune response, highlighting its immunomodulatory role. To assess whether this effect is unique to arazyme, we examined another bacterial metalloprotease, Oligopeptidase A (OpdA).</p><p><strong>Methods: </strong>OpdA was produced and purified. Endotoxin levels were measured. C57BL/6 mice received intravenous B16F10-Nex2 cells, followed by treatments with either active or heat-inactivated OpdA. Pulmonary nodules were counted. Immune cells involved in the response were characterized using FACS and depletion experiments. Cytokines were measured by ELISA and intracellular cytokine analysis. OpdA receptor activation was studied in bone marrow-derived cells from knockout and wild-type mice using inhibitors.</p><p><strong>Results: </strong>Heat-inactivated OpdA significantly reduced metastasis, dependent on tumor-specific CD4+ and CD8+ T cells and IFN-γ, both locally and systemically, with decreased IL-10 levels suggesting a proinflammatory environment. Treatment increased secretion of nitric oxide, IL-12p40, and TNF-α from bone marrow cells via enzymatic activity, involving MyD88/TRIF and MAPK pathways. Conclusion: OpdA shows potential as a tumor vaccine adjuvant, promoting antigen presentation and tumor-specific immune responses.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1630886"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185636","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":"Case Report: Subacute combined degeneration of the spinal cord mimic accompanying adaptor protein-3B2-IgG.","authors":"Ying Liu, Guo-Hui Gao, Jie Lin, Chong Sun, Yan-Yin Zhao","doi":"10.3389/fimmu.2025.1598033","DOIUrl":"10.3389/fimmu.2025.1598033","url":null,"abstract":"<p><p>We here report the first case of subacute combined degeneration (SCD)-mimic accompanying adaptor protein-3B2 (AP3B2) antibody, expanding the clinical spectrum of AP3B2 antibody-associated disorders. A 55-year-old woman presented with progressive limb numbness, gait instability, and sensory ataxia over six years, unresponsive to prolonged vitamin B12 therapy. Neurological examination revealed combined posterior column, lateral column, and peripheral nerve involvement. Cervical spinal MRI demonstrated posterior column hyperintensity, while electrophysiology confirmed sensory-predominant peripheral neuropathy. Anti-AP3B2 antibodies were detected in serum (titer 1:100), with no evidence of vitamin B12 malabsorption, copper deficiency, paraneoplastic syndromes, or other immune abnormalities. Clinically resembling SCD, key discrepancies included: initial mononeuropathy multiplex/sensory neuronopathy evolving into symmetric polyneuropathy; normal vitamin B12 metabolism despite treatment resistance; absence of megaloblastic anemia. Based on AP3B2 expression in dorsal root ganglia, spinal cord, and cerebral cortex, we propose the novel entity \"anti-AP3B2 antibody-associated SCD-mimic phenotype,\" highlighting its distinction from classical SCD. AP3B2 antibodies likely mediate neuronal injury via CD8⁺ T-cell cytotoxicity, consistent with intracellular antigen-targeting autoimmune mechanisms. While prior AP3B2-associated cases primarily featured cerebellar ataxia or sensory ataxia, this case uniquely manifests the SCD-like triad (posterior column, pyramidal tract, and peripheral nerve damage). Clinicians should consider anti-AP3B2 antibody screening in SCD-like patients refractory to vitamin B12 therapy. Although immunotherapy responses remain limited in reported cases, early identification may optimize diagnostic and therapeutic strategies.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1598033"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185535","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":"RIPK1 signaling pathways: implications for autoimmune and neuroinflammatory diseases.","authors":"Abigail Pajulas, Jonathan T Sims, Eric P Hanson, Andrew C Vendel","doi":"10.3389/fimmu.2025.1642593","DOIUrl":"10.3389/fimmu.2025.1642593","url":null,"abstract":"<p><p>Receptor-interacting protein kinase 1 (RIPK1), which regulates cell death and survival pathways, is a promising therapeutic target for the treatment of several autoimmune, inflammatory, and neurodegenerative diseases, having important roles in inflammation, apoptosis, and necroptosis. In this review, we describe recent insights that help elucidate the molecular mechanisms of signaling pathways reliant on RIPK1, focusing on its scaffolding function and kinase activity. We emphasize the cell type-specific effects of RIPK1, characterizing its role in necroptosis, immune cell regulation, and tissue-specific responses. Lastly, we present the relevance of RIPK1 in autoimmune and inflammatory diseases, while highlighting the clinical landscape for RIPK1-targeting therapies. All together, this review aims to present recent findings pertaining to RIPK1 signaling and discuss its potential as a therapeutic target in diseases.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1642593"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185618","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":"Long-term follow-up of patients with relapsed/refractory multiple myeloma after BCMA CAR-T-cell therapy.","authors":"Yuanyuan Hao, Zhen Wang, Lei Zhang, Yanliang Bai, Xiaoli Yuan, Jing Yang, Li Jiang, Junwei Niu, Wei Cheng, Wei Li, Zhoufeng Huang, Yuqing Chen, Kai Sun, Zunmin Zhu","doi":"10.3389/fimmu.2025.1650568","DOIUrl":"10.3389/fimmu.2025.1650568","url":null,"abstract":"<p><strong>Background: </strong>B-cell maturation antigen (BCMA)-directed chimeric antigen receptor (CAR) T-cell therapy has demonstrated potent short-term efficacy in patients with relapsed/refractory multiple myeloma (R/R MM); however, long-term clinical data remain limited. Here, we report extended follow-up outcomes from our single-center experience.</p><p><strong>Methods: </strong>Between August 20, 2018, and December 31, 2021, 11 patients with R/R MM received BCMA-targeted CAR-T-cell therapy at our center. Preconditioning consisted of cyclophosphamide and fludarabine chemotherapy, followed by infusion of 1-5×10⁶ CAR⁺ T cells/kg. We evaluated overall response rate (ORR), long-term efficacy, safety profiles, and their correlations with clinical/disease characteristics.</p><p><strong>Results: </strong>The ORR was 72.7% (8/11), including 6 complete remissions (54.5%) and 2 partial/very good partial remissions. With a median follow-up of 23 months (range: 2-63 months), 75% (6/8) of the responders remained relapse-free, and 4 patients (50%) were alive at the time of data cutoff. The median progression-free survival (PFS) and overall survival (OS) of responders both reached 35 months. In terms of safety, most patients experienced moderate cytokine release syndrome (CRS), with 2 cases of grade 3-4 CRS.</p><p><strong>Conclusion: </strong>BCMA CAR-T-cell therapy exhibits favorable safety and efficacy in advanced R/R MM. Long-term follow-up confirmed durable responses in 50% of the advanced R/R MM patients who responded to the treatment (4/8).</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"16 ","pages":"1650568"},"PeriodicalIF":5.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185433","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}