Tissue Barriers最新文献

{"title":"Pathogenic breaches: how viruses compromise blood-tissue barriers.","authors":"Apoorva, Sunit K Singh","doi":"10.1080/21688370.2025.2549020","DOIUrl":"10.1080/21688370.2025.2549020","url":null,"abstract":"<p><p>Blood-tissue barriers (BTBs) are highly specialized, selectively permeable surfaces that separate the circulatory system from delicate tissues and organs. Critical examples include the blood-brain barrier (BBB), blood-retinal barrier (BRB), blood-testis barrier (BTB), and other organ-specific barriers, including the alveolar-capillary interface in the lungs and the glomerular filtration barrier in the kidneys. These barriers regulate the bidirectional transport of nutrients, gases, and waste while restricting pathogens, toxins, and immune cells to maintain physiological balance. Nevertheless, viruses have evolved multiple strategies to circumvent or compromise these barriers, facilitating viral entry, evading immune surveillance, and establishing infection within protected compartments. Neurotropic viruses, including the West Nile virus and Japanese encephalitis virus, impair the blood-brain barrier by disrupting tight junction proteins and cytokine storms. In contrast, respiratory viruses such as influenza and SARS-CoV-2 affect the lung barrier, resulting in alveolar injury and systemic inflammation. Other viruses, such as the Zika virus, affect the BTB and placental barriers, presenting significant risks to fetal development and reproductive health. Such breaches facilitate viral spread, exacerbate tissue damage, and complicate therapeutic interventions. This review provides a comprehensive overview of blood-tissue barrier architecture, function, and mechanisms of viral disruption, highlighting their dual role in protection and susceptibility during viral infections. By elucidating interactions between viruses and blood-tissue barriers, this work highlights emerging research directions to mitigate viral pathogenesis and enhance treatment efficacy for barrier-associated diseases.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2549020"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144970867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patient-derived 3D nasal spheroids reveal epithelial changes following Dupilumab therapy in CRSwNP: a preliminary report.","authors":"Nadia Lobello, Giovanna Lucia Piazzetta, Corrado Pelaia, Mariaimmacolata Preianò, Nicola Lombardo, Emanuela Chiarella","doi":"10.1080/21688370.2025.2552004","DOIUrl":"10.1080/21688370.2025.2552004","url":null,"abstract":"<p><p>Chronic rhinosinusitis with nasal polyps (CRSwNP) is a type 2 inflammatory disease associated with epithelial dysfunction and impaired mucosal barrier integrity. Dupilumab, an IL-4 receptor alpha antagonist, has shown clinical efficacy, but its cellular effects on nasal epithelium remain poorly understood. Advanced in vitro models such as 3D spheroid cultures may provide insight into epithelial organization under treatment. We conducted a preliminary study using nasal epithelial cells obtained from three patient groups: CRSwNP treated with Dupilumab for 16 weeks (<i>n</i> = 3), untreated CRSwNP (<i>n</i> = 3), and turbinate hypertrophy controls (<i>n</i> = 3). Cells were isolated by enzymatic digestion and cultured in ultra-low attachment plates using sphere-promoting medium to assess spheroid formation. Observations were performed using phase-contrast microscopy. Due to the limited sample size, data were analyzed qualitatively without statistical testing. Control cells formed compact spheroids, while untreated CRSwNP cells failed to generate structured spheroids, showing only aggregates. Cells from Dupilumab-treated patients produced well-organized spheroids, suggesting improved epithelial organization. Occasional surface movement was observed but not quantitatively assessed. No molecular or ultrastructural assays were performed to confirm mechanistic hypotheses. Our preliminary findings indicate that Dupilumab treatment may be associated with improved epithelial organization in CRSwNP, as shown by spheroid formation in 3D culture. However, these observations are preliminary and based on a small cross-sectional cohort. Future studies should include longitudinal sampling, functional assays, and molecular analyses to confirm mechanisms and validate these results.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2552004"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144970945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intestinal epithelial cells in health and disease.","authors":"Chenchen An, Chonggui Jiang, Wangxiang Pei, Ao Li, Minghui Wang, Yufei Wang, Hua Wang, Li Zuo","doi":"10.1080/21688370.2025.2504744","DOIUrl":"10.1080/21688370.2025.2504744","url":null,"abstract":"<p><p>This comprehensive review delves into the pivotal role of intestinal epithelial cells in the context of various diseases. It provides an in-depth analysis of the diverse types and functions of these cells, explores the influence of multiple signaling pathways on their differentiation, and elucidates their critical roles in a spectrum of diseases. The significance of the gastrointestinal tract in maintaining overall health is extremely important and cannot be exaggerated. This complex and elongated organ acts as a crucial link between the internal and external environments, making it vulnerable to various harmful influences. Preserving the normal structure and function of the gut is essential for well-being. Intestinal epithelial cells serve as the primary defense mechanism within the gastrointestinal tract and play a crucial role in preventing harmful substances from infiltrating the body. As the main components of the digestive system, they not only participate in the absorption and secretion of nutrients and the maintenance of barrier function but also play a pivotal role in immune defense. Therefore, the health of intestinal epithelial cells is of vital importance for overall health.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2504744"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The gatekeepers breached: claudin dysregulation in psychiatric disorders.","authors":"Tarek Ziad Arabi, Wael Alkattan, Belal Nedal Sabbah, Abderrahman Ouban","doi":"10.1080/21688370.2026.2616111","DOIUrl":"10.1080/21688370.2026.2616111","url":null,"abstract":"<p><p>Psychiatric disorders such as depression, bipolar disorder, schizophrenia, and autism spectrum disorder are increasingly understood not only as disruptions in brain chemistry or circuitry but also as disorders of neural microenvironments and barriers. This review explores the critical role of claudins, transmembrane proteins that form tight junctions, in maintaining the integrity of the blood - brain barrier (BBB) and other brain structures. Claudin-5, prominently expressed in the BBB, and claudin-11, essential for myelin integrity, emerge as central players in psychiatric pathophysiology. Evidence from human postmortem studies, serum biomarkers, and animal models indicates that claudin-5 is downregulated in key brain regions in depression, bipolar disorder, and schizophrenia, contributing to BBB permeability and facilitating neuroinflammation. Similarly, claudin-11 deficits in schizophrenia suggest impaired myelination and disrupted neural connectivity. In autism and ADHD, altered tight junction protein profiles imply more subtle or context-dependent barrier dysfunction. Mechanistically, claudin dysregulation permits peripheral inflammatory mediators and immune molecules to access brain tissue, triggering neuroinflammation, oxidative stress, and synaptic dysfunction. Additionally, loss of myelin barrier function may impair signal timing and synchronization. These findings support a unifying hypothesis: that barrier dysfunction, mediated by claudin disruption, underlies diverse psychiatric symptoms by destabilizing the brain's protected environment. Recognizing the role of claudins in mental illness opens avenues for novel biomarker development and therapeutic strategies aimed at restoring barrier integrity, offering a new perspective on the intersection of neurobiology and psychiatry.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2616111"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced 3D-Printed hydrogel dressings incorporating platelet-rich plasma for accelerated skin repair.","authors":"Carlos de Almeida Barbosa, Luize Kremer Gamba, Rossana Baggio Simeoni, Maria Fernanda Villaça Koch, Marco Andre Cardoso, Ricardo Correa Cunha, Luiz Cesar Guarita-Souza, Julio Cesar Francisco, Beatriz Luci Fernandes","doi":"10.1080/21688370.2025.2537992","DOIUrl":"10.1080/21688370.2025.2537992","url":null,"abstract":"<p><p>The restoration of cutaneous barrier function following deep skin injury remains a critical challenge in regenerative medicine. In this study, we developed a semi-occlusive wound dressing by combining sodium alginate hydrogel with platelet-rich plasma (PRP), using 3D bioprinting technology to ensure structural precision and consistent bioactive distribution. This hybrid system was engineered to support tissue repair by enhancing re-epithelialization, stimulating angiogenesis, and promoting organized extracellular matrix remodeling. In vivo experiments using full-thickness skin wounds in mice revealed that the PRP enriched dressings accelerated wound contraction and epithelial closure, especially during the early stages of healing. Histological analyses showed increased formation of capillary-like structures, a shift toward type I collagen dominance, and reduced inflammation in PRP treated groups. These effects point to a more mature and functional regenerative process. Importantly, the combination of PRP with a bioprinted hydrogel scaffold not only facilitated structural recovery but also contributed to restoring the physiological integrity of the skin barrier. This approach offers a low-cost and adaptable platform with strong translational potential for the treatment of complex skin wounds.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2537992"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Robust paraffin embedding of 3D cultured vocal fold epithelial organoids.","authors":"Yun-Lan Yi, Hong Zhang, Ying-Ying Wang, Ping-Ping Cao, Bao-Feng Wang","doi":"10.1080/21688370.2025.2583560","DOIUrl":"10.1080/21688370.2025.2583560","url":null,"abstract":"<p><p>Vocal fold organoids recapitulate critical structural and functional features of native vocal fold mucosa, providing a physiologically relevant model for investigating vocal fold biology and disease mechanisms. However, conventional histological processing of these organoids remains technically demanding, often resulting in substantial sample loss, inadequate visualization during embedding and difficult retrieval the blocks from Eppendorf tubes. To address these issues, we established a comprehensive protocol that integrates direct eosin pre-staining, agarose pre-embedding and fine-needle-assisted retrieval of agarose-embedded blocks. This optimized workflow increases processing efficiency, enables enhanced visual monitoring and better preserves cytoarchitectural integrity. Consequently, sectioning is facilitated, and both hematoxylin and eosin (HE) staining and immunofluorescence (IF) exhibit superior quality and reproducibility, producing highly consistent morphological details and robust signal resolution. The proposed method provides a standardized and reliable platform for high-resolution histological and IF examination of epithelial organoids, thereby extending its utility in vocal fold research and related organoid applications.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2583560"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13228971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145432176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabinoid/lysophosphatidylinositol-sensing G-protein coupled receptor 55 promotes intestinal tight junction assembly and its mechanistic insights.","authors":"Supisara Treveeravoot, Pichayapa Sukmak, Pimngeon Chatkul, Apiwan Arinno, Suchanan Amonsiriwit, Pitsinee Supapol, Thaam Limwattananon, Nuttakritta Choksukchalalai, Natnicha Kitti-Udom, Nichapa Chindaduangratn, Wanapas Wachiradejkul, Wilasinee Satianrapapong, Jaturon Kwanthongdee, Aekkacha Moonwiriyakit, Chatchai Muanprasat, Pawin Pongkorpsakol","doi":"10.1080/21688370.2025.2585726","DOIUrl":"10.1080/21688370.2025.2585726","url":null,"abstract":"<p><p>Intestinal tight junction disruption initiates progression of related diseases including inflammatory bowel disease (IBD) with no FDA-approved drug for tight junction recovery. To demonstrate the effect of pharmacological activation of the cannabinoid/lysophosphatidylinositol-sensing G-protein coupled receptor 55 (GPR55) by its specific synthetic agonist O1602 on intestinal barrier function, tight junction-dependent permeability, and its underlying mechanisms. We show that O1602 treatment increased transepithelial electrical resistance (TER) across intestinal epithelial-like T84 cell monolayers and suppressed 4-kDa FITC-dextran permeability. Neither CB1 inhibitor nor CB2 inhibitor has affected TER increases in response to O1602 treatment. O1602 was ineffective in enhancing intestinal barrier integrity in T84 monolayers treated with GPR55 antagonist or in GPR55 KD T84 monolayers, indicating that GPR55 agonism promotes intestinal barrier function and inhibits tight junction-dependent leak pathway permeability. In fact, O1602 treatment also prevented TNF-α-induced intestinal barrier disruption in IFN-γ-primed T84 and Caco-2BBe monolayers. The effect of O1602 treatment on enhancing TER across T84 cell monolayers was abolished by pre-treatment with inhibitors of PLC, CaMKKβ, AMPK, SIRT-1, ERK, PKA, β-arrestin, and mTOR. In addition, O1602 failed to promote TER increases in SIRT-1 KO T84 monolayers. Our data from western blot analysis, SIRT-1 activity assay, and immunofluorescence staining of tight junction proteins, coherently recapitulates that GPR55 agonism induces intestinal tight junction assembly via PLC/[Ca²⁺]_i/CaMKKβ/AMPK/SIRT-1/ERK-dependent mechanism. Hence, we furnish the first line of evidence supporting that GPR55 is the regulator of tight junction in intestinal epithelial monolayers and may serve as a novel class of therapeutic target for tight junction disruption-associated diseases.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2585726"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145496670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Alzheimer's associated Aβ oligomers and oxidative stress on blood-brain barrier dysfunction.","authors":"Brittany E Watson, Mihyun L Waugh, Nolan J Foreman, Melissa A Moss","doi":"10.1080/21688370.2025.2553927","DOIUrl":"10.1080/21688370.2025.2553927","url":null,"abstract":"<p><p>Blood-brain barrier (BBB) dysfunction is an early event observed in Alzheimer's disease (AD). Two characteristics of AD brain and brain vasculature contribute to BBB dysfunction: the accumulation of aggregated amyloid-β protein (Aβ) and an increase in oxidative stress. This work uses a BBB model of primary human brain microvascular endothelial cells to investigate the individual and synergistic influence of both pathogenic Aβ oligomers and oxidative stress on BBB transendothelial electrical resistance (TEER), an indicator of barrier integrity. Results indicate that nontoxic, physiological concentrations of Aβ oligomers reduce TEER, while Aβ monomer remains inert. Moreover, introducing mild oxidative stress, which alone does not influence monolayer integrity, exacerbates the effect of Aβ oligomers on TEER within this BBB model. These findings advance the understanding of BBB dysfunction in AD and point toward therapeutic strategies targeting this early event that contributes to a currently irreversible disease.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2553927"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paracrine signaling mediators of vascular endothelial barrier dysfunction in sepsis: implications for therapeutic targeting.","authors":"Shahid Puthiyottil, Tom Skaria","doi":"10.1080/21688370.2025.2503523","DOIUrl":"10.1080/21688370.2025.2503523","url":null,"abstract":"<p><p>Vascular endothelial barrier disruption is a critical determinant of morbidity and mortality in sepsis. Whole blood represents a key source of paracrine signaling molecules inducing vascular endothelial barrier disruption in sepsis. This study analyzes whole-genome transcriptome data from sepsis patients' whole blood available in the NCBI GEO database to identify paracrine mediators of vascular endothelial barrier dysfunction, uncovering novel insights that may guide drug repositioning strategies. This study identifies the regulated expression of paracrine signaling molecules TFPI, MMP9, PROS1, JAG1, S1PR1, and S1PR5 which either disrupt or protect vascular endothelial barrier function in sepsis and could serve as potential targets for repositioning existing drugs. Specifically, TFPI (barrier protective), MMP9 (barrier destructive), PROS1 (barrier protective), and JAG1 (barrier destructive) are upregulated, while S1PR1 (barrier protective) and S1PR5 (barrier protective) are downregulated. Our observations highlight the importance of considering both protective and disruptive mediators in the development of therapeutic strategies to restore endothelial barrier integrity in septic patients. Identifying TFPI, MMP9, PROS1, JAG1, S1PR1, and S1PR5 as druggable paracrine regulators of vascular endothelial barrier function in sepsis could pave the way for precision medicine approaches, enabling personalized treatments that target specific mediators of endothelial barrier disruption to improve patient outcomes in sepsis.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2503523"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144080651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Permeation of small extracellular vesicles across a human blood-brain barrier transwell model remains below particle detection limits, even under oxygen/glucose deprived conditions.","authors":"Adrián Klepe, Sonja Damberger, Ana Špilak, Andreas Brachner, Winfried Neuhaus","doi":"10.1080/21688370.2025.2610016","DOIUrl":"10.1080/21688370.2025.2610016","url":null,"abstract":"<p><p>Ischemic stroke disrupts blood-brain barrier (BBB) integrity and alters small extracellular vesicle (sEV) signaling, yet the mechanisms underlying sEV transport across compromised barriers remain poorly understood. This study investigated BBB-sEV interactions under normal and stroke-mimicking oxygen/glucose deprivation (OGD) conditions using an <i>in vitro</i> human BBB co-culture model consisting of brain capillary endothelial (BCECs, hCMEC/D3) and astrocytoma cells (1321N1). Model characterization revealed that co-culture with 1321N1 cells enhanced BBB vulnerability to OGD compared to hCMEC/D3 mono-culture. OGD exposure (5 h and 24 h) progressively decreased transendothelial electrical resistance (TEER) and increased FITC-dextran 4 (FD4) permeability, with more severe impairment in co-cultures (e.g. TEER - after 5 h: 0.85-fold, after 24 h: 0.55-fold for co-culture related to mono-culture). Following 19 h oxygen and glucose restoration ('recovery') after 5 h OGD, barrier integrity loss was halted but not reversed. Transcriptomic analysis revealed adaptive cellular responses including upregulated glucose transporter 1 (GLUT1) and vascular endothelial growth factor (VEGF), alongside temporal changes in tight junction protein expression (CLDN5, CDLN6). sEV secretion kinetics in apical and basolateral compartments demonstrated that both cell types released particles in response to OGD in a time-dependent manner, with co-cultures showing enhanced secretion compared to mono-cultures. sEV uptake and permeation studies using eight cancer cell line-derived sEVs revealed cell-origin dependent internalization patterns by BCECs, with the highest uptake for HEK293T and SH-SY5Y sEVs. These internalized sEVs were predominantly targeted to lysosomes. Despite severe barrier disruption due to OGD transcellular permeation of single sEV particles was not detectable.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2610016"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145935324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}