International Journal of Oral Science最新文献

{"title":"Ameloblastin amphipathic helix motif mediates ameloblast polarization and prismatic enamel formation","authors":"Gayathri Visakan, Rucha Arun Bapat, Jing Cai, Ethan Trevor Suwandi, Derk Joester, Natalie C. Kegulian, Edwin Sarkisians, Marziyeh Aghazadeh, Simon Webster, Janet Moradian-Oldak","doi":"10.1038/s41368-026-00457-0","DOIUrl":"https://doi.org/10.1038/s41368-026-00457-0","url":null,"abstract":"Ameloblastin (Ambn) is a tooth-specific multifunctional protein essential for enamel biomineralization and the formation of its prismatic microstructure. To examine the function of the evolutionarily conserved cell-binding Ambn amphipathic helix (AH) motif, we deleted the hydrophobic residues within the Ambn AH motif in genetically engineered mice. Enamel in the homozygous (AmbnΔL76-P86) mutants had normal thickness but was hypo-mineralized and lacked prismatic structure. Micro-CT analysis further revealed that both the secretory and maturation stages of amelogenesis were delayed and proceeded slower than in the controls. Ameloblasts in the mutants were stunted and exhibited loss of cell polarity, as demonstrated by the mislocalization of Pard3, Claudin-1 and GM130 immunosignals. In the AmbnΔL76-P86 mutants, a loss of Ambn-ameloblast distal membrane interaction was observed, with nuclear localization of β-catenin and p-Smad2/3, and a decrease in RhoA immunolabeling intensity, suggesting that changes in known signaling pathways may connect Ambn-cell interactions to the establishment of cell polarity. Together, these findings support a model in which AH-dependent Ambn engagement at the distal ameloblast membrane contributes to secretory-stage polarity and prism patterning, with downstream consequences for enamel organization and maturation-stage mineral density.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"24 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of integrin β1 and discoidin domain receptor 2 in cranial regeneration and skeletal progenitor cell function","authors":"Yuanyuan Han, Chunxi Ge, Rajay A. Kamath, Vesa Kaartinen, Renny T. Franceschi","doi":"10.1038/s41368-026-00455-2","DOIUrl":"https://doi.org/10.1038/s41368-026-00455-2","url":null,"abstract":"The two principal collagen receptors in bone, the collagen-binding β1 integrins and discoidin domain receptor 2 (DDR2), each have important roles in development, but their functions in bone regeneration are largely unexplored. Using a critical-size calvarial defect model, we assessed the relative roles of these two receptor classes in BMP2-induced regeneration using a conditional knockout approach where Itgb1 (encodes integrin β1) and/or Ddr2 were selectively inactivated in GLI1+ skeletal progenitor cells (SPCs). Inactivating either Itgb1 or Ddr2 partially inhibited calvarial regeneration, while inactivation of both receptors almost completely blocked bone healing. Responses were linked to reduced proliferation and migration of GLI1+ SPCs into defects and reduced endochondral and intramembranous bone formation. To examine the consequences of receptor inactivation at the cellular level, calvarial SPCs lacking Itgb1, Ddr2 or both receptors were generated. Loss of either receptor inhibited osteoblast differentiation, migration, cell spreading, focal adhesion formation, and nuclear localization of the mechanotransducer, YAP1. Importantly, inactivation of both receptors inhibited responses to a greater extent than was seen with individual knockouts. Interestingly, while inactivation of one allele of either Itgb1 (Itgb1fl/+) or Ddr2 (Ddr2fl/+) did not affect any of the above parameters, inactivation in double heterozygotes (Itgb1fl/+ ;Ddr2fl/+) was strongly inhibitory, which is indicative of a genetic interaction between Itgb1 and Ddr2. Lastly, immunofluorescence and immunoprecipitation analysis suggest that DDR2 and ITGB1 physically interact, providing a potential explanation for the observed functional cooperativity. These studies provide a mechanistic basis for bone regeneration strategies involving combined activation of integrin β1 and DDR2.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"8 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporally regulated FGFR2-retinoic acid signaling mediates dura mater-suture mesenchyme interactions to prevent craniosynostosis in mice.","authors":"Lu Gao, Peng Chen, Jifan Feng, Tingwei Guo, Mingyi Zhang, Thach-Vu Ho, Jian-Fu Chen, Yang Chai","doi":"10.1038/s41368-026-00449-0","DOIUrl":"10.1038/s41368-026-00449-0","url":null,"abstract":"<p><p>Congenital anomalies often arise during critical developmental time windows, yet the underlying mechanisms remain unclear. Here, we identify a time-specific FGFR2-retinoic acid signaling axis regulating postnatal coronal suture development through dura mater-suture mesenchyme interactions. FGFR2 signaling gradually declines after birth, leading to reduced retinoic acid signaling by moderating the expression of Aldh1a3 in the dura mater and suture mesenchyme alongside that of Rbp1 in the dura mater, thereby preserving GLI1+ progenitors and restraining osteogenesis to maintain suture patency. Importantly, FGFR2 overactivation in Fgfr2IIIc mutant mice within an early time window, disrupts this physiological FGFR2-retinoic acid signaling decline by upregulating Rbp1 and Aldh1a3 through enhanced P38 signaling. This leads to increased retinoic acid synthesis, premature osteogenic differentiation of GLI1+ progenitors, and coronal suture craniosynostosis. Significantly, genetic restoration of retinoic acid signaling rescues craniosynostosis in Fgfr2IIIc mutant mice, confirming retinoic acid signaling as a key downstream effector of FGFR2 signaling. Notably, restoration of suture patency alone rescues neurocognitive dysfunctions in Fgfr2IIIc mutant mice despite Fgfr2 mutation in the brain, demonstrating that the neurocognitive impairments primarily arise from cranial structural constraints and elevated intracranial pressure rather than intrinsic neural defects. This critical postnatal time window in mice parallels the timing of FGFR2-related craniosynostosis onset in humans, underscoring the importance of this study in advancing our understanding of the molecular and cellular mechanisms in craniosynostosis. Our findings define a temporally regulated FGFR2-P38-retinoic acid signaling axis and highlight retinoic acid signaling as a promising therapeutic target in FGFR2 overactivation-related craniosynostosis.</p>","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":""},"PeriodicalIF":17.6,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13478313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis","authors":"Jiawei Lu, Xiao Wu, Zehui Xiong, Jinyi Zhang, Haipeng Yang, Feng Liu, Lijun Luo","doi":"10.1038/s41368-026-00450-7","DOIUrl":"https://doi.org/10.1038/s41368-026-00450-7","url":null,"abstract":"Lymphocytes play a central role in adaptive immunity and represent the primary source of RANKL in periodontitis. Understanding their organization and activation within gingiva is therefore essential. This study investigates the role of tertiary lymphoid structures (TLSs), ectopic lymphoid aggregates that orchestrate local immune responses. Using multiplex immunohistochemistry staining, we found that TLSs form and mature with increasing inflammatory severity. These structures function as hubs for B cell activation and were associated with poorer surgical outcomes. Given the known role of fibroblasts in initiating TLS assembly, we explored the underlying mechanism. Using single-cell RNA sequencing and in vitro assays, we identified that oral pathogens activate the IFN-I–IRF7 axis in gingival fibroblasts, leading to overproduction of IFNβ and driving their differentiation into a CXCL13-producing subtype that facilitates TLS organization. Furthermore, in a mouse periodontitis model, we demonstrated that activated IgD+CD80+ B cells within TLSs promote osteoclastogenesis and bone resorption via RANKL secretion. Therapeutically, inhibition of IFN-I signaling disrupted this pathogenic cascade by suppressing TLS formation and subsequent RANKL production, thereby mitigating periodontitis bone loss. In conclusion, our findings establish TLSs as pathological hubs that coordinate B cell-mediated bone destruction in periodontitis and highlight the IFN-I signaling pathway as a promising target for therapeutic intervention.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"19 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148587299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing pulp regeneration through metabolic reprogramming of mature dental pulp stem cells mediated by GLUT1/HK2 mRNA delivery.","authors":"Tiankai Di, Yuhan Liu, Zhili Li, Lulu Wang, Peiyi Li, Meng Nian, Dezhong Zhou, Lina Niu, Yujiang Chen","doi":"10.1038/s41368-026-00452-5","DOIUrl":"10.1038/s41368-026-00452-5","url":null,"abstract":"<p><p>The age-related decline in the pro-angiogenic capacity of mature dental pulp stem cells (DPSCs) severely limits pulp regeneration. We identify impaired glycolytic metabolism, driven by reduced glucose transporter type 1 (GLUT1) and hexokinase 2 (HK2) expression, as the key mechanism, as its inhibition diminished endothelial tube formation. To reverse this, we developed an aminolyzed highly branched poly(β-amino ester) (HBPA) as a vector for GLUT1/HK2 mRNA co-delivery, achieving >90% transfection efficiency with excellent biocompatibility. In vitro, conditioned medium from reprogrammed mature DPSCs resulted in a 2.0-fold increase in capillary length and a 2.3-fold increase in branch points, restoring angiogenic potential to levels equivalent to those of immature DPSCs. This efficacy translated robustly in vivo, where a tooth root slice model showed reprogrammed cells generated tissue with a vessel density of 10.2 vessels per mm², 2.5-fold higher than that of untreated controls. Crucially, this level of vascularization was statistically indistinguishable from that achieved by the benchmark immature DPSCs. Our study demonstrates that HBPA-mediated metabolic reprogramming effectively rejuvenates mature DPSCs by restoring the \"Metabolic-ECM-Angiogenesis Axis\", offering a translatable strategy for predictable, vascularized pulp regeneration.</p>","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":""},"PeriodicalIF":17.6,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author Correction: KDM6B/Pdk1 glycolytic pathway-driven ZEB2 lactylation promotes cellular cementum formation.","authors":"Zhengkun Yang, Huiyi Wang, Junhong Xiao, Qiudong Yang, Jiahui Sun, Heyu Liu, Zhendong Huang, Li Ma, Xin Huang, Chuan Wang, Xiaoxuan Wang, Zhengguo Cao","doi":"10.1038/s41368-026-00453-4","DOIUrl":"10.1038/s41368-026-00453-4","url":null,"abstract":"","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":""},"PeriodicalIF":17.6,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13373174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P. gingivalis-host interactions direct antibiotic adjuvants for periodontitis antimicrobial therapy.","authors":"Xiya Liu,Zuoying Yuan,Zhuo Wan,Xiaojing Yuan,Yue Wang,Yike Gao,Linxue Zhang,Rui Song,Jingyi Sang,Yang Wang,Yiming Han,Yuming Zhao,Cun-Yu Wang","doi":"10.1038/s41368-026-00448-1","DOIUrl":"https://doi.org/10.1038/s41368-026-00448-1","url":null,"abstract":"Porphyromonas gingivalis (P. gingivalis) invades host cells to evade antibiotics, driving the recurrence of periodontitis. However, current clinical treatment strategies remain ineffective in addressing this intracellular invasion by the bacteria. Here, we report a host-directed strategy that blocks bacterial invasion by targeting key host factors, including collagen I (using FT011), lipid rafts (using simvastatin), integrin β1 (using ATN-161), and FAK signaling (using YH-306). Inhibiting these targets significantly reduced P. gingivalis infection in human oral keratinocytes and periodontal ligament stem cells. Crucially, simvastatin restored the osteogenic ability of P. gingivalis-infected PDLSCs. These drugs subsequently functioned as effective antibiotic adjuvants. The combination of simvastatin or YH-306 with metronidazole, a standard-of-care antibiotic for periodontitis, exhibited potent synergistic effects, significantly eradicating intracellular bacteria at reduced antibiotic dosages. In a rat periodontitis model, simvastatin-metronidazole therapy yielded superior outcomes, significantly mitigating bacterial load, inflammation, and alveolar bone loss. The repurposing of clinically available drugs, such as simvastatin, as antibiotic adjuvants represents a promising, readily translatable therapeutic approach for periodontitis.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"35 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148416002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHAC2-mediated glutathione metabolic reprogramming drives N1 polarization of bone marrow neutrophils and exacerbates inflammatory comorbidities.","authors":"Yuting Niu,Yuman Li,Shiyu Sun,Chenyu Deng,Fan He,Yiming Chen,Tiansong Xu,Zhewen Hu,Gai Yang,Leran Li,Boon Chin Heng,Yan Lv,Ying Huang,Xuliang Deng","doi":"10.1038/s41368-026-00451-6","DOIUrl":"https://doi.org/10.1038/s41368-026-00451-6","url":null,"abstract":"The proinflammatory (N1) polarization of bone marrow (BM) neutrophils, driven by central immune remodeling in response to peripheral inflammation, plays a critical role in propagating localized inflammatory conditions, such as periodontitis, to systemic levels. Although this process involves metabolic reprogramming, the specific underlying metabolic mechanisms of neutrophil N1 polarization within the periodontitis-modified BM niche remain poorly defined. Integrated transcriptomic and metabolomic analyses in this study revealed that periodontitis reprograms intracellular glutathione (GSH) metabolism in BM neutrophils, facilitating their N1 polarization. Central to this mechanism is the upregulation of Chac2, an enzyme that promotes GSH accumulation. This enhancement is accompanied by elevated GSH redox cycling, which supports sustained ROS production and NET formation, thereby amplifying inflammatory responses. We further identified type I interferon (IFN-I) signaling as a key upstream regulator that induces Chac2 expression and drives metabolic reprogramming. Importantly, the intraosseous delivery of AAV-delivered Chac2 shRNA in db/db mice with periodontitis markedly reduced neutrophil-aggravated systemic inflammatory comorbidity symptoms and improved glycemic control, underscoring the functional relevance of this pathway in diabetic comorbidity. Together, these findings thus delineate the IFN-I-Chac2-GSH axis as a core signaling mechanism regulating neutrophil N1 polarization in the BM niche, providing new insights into how periodontal inflammation reprograms immune functions at the systemic level. This study thus broadens the conceptual framework of neutrophil immunometabolism and proposes targeting the Chac2-GSH axis as a potential therapeutic strategy for systemic comorbidities associated with periodontitis.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"22 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148416001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory myofibroblasts reprogram neutrophil fate to drive chronic inflammation in peri-implantitis","authors":"Weimin Lin, Bassam A. Altayar, Shuang Jiang, Kun He, Yi Zhao, Qingheng Wu, Yumeng Lin, Malcolm Xing, Quan Yuan","doi":"10.1038/s41368-026-00447-2","DOIUrl":"https://doi.org/10.1038/s41368-026-00447-2","url":null,"abstract":"Peri-implantitis (PI) is a multifactorial chronic inflammatory disease characterized by persistent mucosal inflammation and progressive marginal bone loss, yet the tissue architecture and cellular programs that sustain chronic inflammation remain incompletely defined. Here, we integrate single-cell and spatial transcriptomic analyses with targeted validation to map the PI microenvironment and its regulatory circuits. PI lesions exhibit marked immune enrichment, including expansion of CXCR4⁺ aged neutrophils with enhanced survival signaling consistent with apoptosis delay. Spatial and communication analyses reveal a PI-specific stromal–myeloid organization in which fibroblast-rich regions are closely associated with myeloid hotspots and display heightened CXCL- and CSF-related signaling. Within the fibroblast compartment, inflammatory myofibroblasts emerge as a prominent predicted source within a CXCL/CSF-enriched secretory program, with CXCL6 and CSF3 highlighted as candidate mediators of neutrophil recruitment and survival. Functionally, blockade of the CXCR2 axis reduces neutrophil infiltration and mitigates peri-implant bone resorption. Upstream regulatory analyses nominate STAT4 as a candidate upstream regulator of the inflammatory stromal program; pharmacologic perturbation with lisofylline reduces CXCL6/CSF3 expression, weakens neutrophil chemotaxis, partially restores apoptosis sensitivity, and alleviates inflammation and bone loss in vivo. Together, these findings support a stromal–neutrophil circuit that sustains chronic inflammation in PI and highlight stromal inflammatory programs and neutrophil recruitment/survival pathways as potential therapeutic entry points.","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"63 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148355628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The YTHDC1-m⁶A-GADD45B axis promotes chondrogenesis of hPDLSCs via suppressing senescence through p53/p21 signalling pathway.","authors":"Dan Tan, Qianke Tao, Luwen Ye, Xuemei Long, Qiaonan Ye, Qilin Li, Jinlin Song, Jingang Xiao","doi":"10.1038/s41368-026-00441-8","DOIUrl":"10.1038/s41368-026-00441-8","url":null,"abstract":"<p><p>Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease with limited therapeutic options. Stem cell-based tissue engineering, particularly utilizing human periodontal ligament stem cells (hPDLSCs), represents a promising approach for cartilage regeneration. However, we have previously demonstrated that chronic inflammation and hypoxic stress in the TMJOA microenvironment markedly accelerate cellular senescence in hPDLSCs, severely impairing their regenerative potential. Here, we identify the YTHDC1-m⁶A-GADD45B axis as a critical regulator of senescence and chondrogenic differentiation in hPDLSCs. We show that YTHDC1, an m⁶A reader protein, is downregulated under inflammatory and senescent conditions. Functional studies reveal that YTHDC1 overexpression attenuates senescence and enhances chondrogenesis, whereas its knockdown exacerbates senescence and suppresses differentiation. Mechanistically, YTHDC1 recognizes m⁶A modifications on GADD45B mRNA and promotes its decay, leading to inhibition of the p53/p21 signaling pathway. Mutation of the m⁶A site in GADD45B abolishes the regulatory effects of YTHDC1. In rats with TMJOA, transplantation of YTHDC1-overexpressing hPDLSCs ameliorated disease phenotypes, an effect reversed by co-expression of wild-type GADD45B. Our findings reveal a novel epitranscriptomic mechanism that regulates hPDLSCs senescence and subsequently affects chondrogenic differentiation, and highlight the therapeutic potential of targeting the YTHDC1-GADD45B-p53/p21 axis.</p>","PeriodicalId":14191,"journal":{"name":"International Journal of Oral Science","volume":"18 1","pages":""},"PeriodicalIF":17.6,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13269875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148258099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}