Frontiers in Cell and Developmental Biology最新文献

{"title":"The role and regulatory mechanisms of the TCA cycle in early embryonic development.","authors":"Yipan Lai, Xiurong Gao, Liwen Zhao, Jin Liu, Chao Gao, Qingfu Yan, Yangneng Zeng, Zibing Liao, Jianing Zhong","doi":"10.3389/fcell.2025.1662431","DOIUrl":"10.3389/fcell.2025.1662431","url":null,"abstract":"<p><p>The tricarboxylic acid cycle (TCA cycle) serves as a critical metabolic hub in embryonic development. Its dynamic reprogramming not only coordinates energy supply and biosynthesis but also profoundly influences cell fate decisions through the metabolic-epigenetic coupling mechanism. This review systematically explores the TCA cycle central role in driving the adaptive metabolic changes of embryos, such as mitochondrial maturation and lineage differentiation, and precisely regulating the timing of zygotic genome activation (ZGA). It highlights how the nuclear translocation of key enzymes in the TCA cycle creates a nuclear metabolic microenvironment, which directly regulates histone modifications (acetylation, methylation) and DNA demethylation through intermediate products like Ac-CoA and α-ketoglutarate (α-KG), thereby achieving epigenetic remodeling. Additionally, the review emphasizes the pathological mechanisms by which mitochondrial dysfunction (such as insufficient ATP synthesis, abnormal metabolite accumulation, and oxidative stress imbalance) leads to developmental arrest through epigenetic disorders and DNA damage.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1662431"},"PeriodicalIF":4.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Survival prediction for Philadelphia chromosome-like acute lymphoblastic leukemia by machine learning analysis: a multicenter cohort study.","authors":"Xiao-Dan Song, Dan-Na Lin, Lv-Hong Xu, Li-Ying Liu, Chi-Kong Li, Xiao-Rong Lai, Ya-Ting Zhang, Wu-Qing Wan, Xiao-Li Zhang, Xiang Lan, Xing-Jiang Long, Bei-Yan Wu, Qi-Wen Chen, Li-Hua Yang, Yun-Yan He","doi":"10.3389/fcell.2025.1650810","DOIUrl":"10.3389/fcell.2025.1650810","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to develop an efficient survival model for predicting event-free survival (EFS) in patients with Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL).</p><p><strong>Methods: </strong>Data related to Ph-like ALL were collected from the South China Children's Leukemia Group (SCCLG) multicenter study conducted from October 2016 to July 2021. A model for predicting the survival of patients with Ph-like ALL was built using Cox proportional hazards regression, random forest, extreme gradient boosting, and gradient boosting machine techniques. By integrating indicators including the concordance index (C-index), 1-, 3-, and 5-year area-under-the-receiver operating characteristics curve (AUROC), Brier score, and decision curve analysis, the predictive capabilities of each model were compared.</p><p><strong>Results: </strong>The random forest algorithm demonstrated the most robust predictive performance. In the test set, the C-index of the random forest model was 0.797 (95% CI: 0.736-0.821; P < 0.001). The AUROCs for 1, 3, and 5 years were 0.787 (95% CI: 0.62-0.953; P < 0.001), 0.797 (95% CI: 0.589-1; P < 0.001), and 0.861 (95% CI: 0.606-1; P < 0.001), respectively. The Brier scores for 1, 3, and 5 years were 0.102 (95% CI: 0.032-0.173; P < 0.001), 0.126 (95% CI: 0.063-0.19; P < 0.001), and 0.121 (95% CI: 0.051-0.19; P < 0.001), respectively.</p><p><strong>Conclusion: </strong>The random forest model effectively predicted the survival outcomes of patients with Ph-like ALL, which can aid clinicians to conduct personalized prognosis assessments in advance. Based on a web-based calculator, using random forest prediction models to calculate the prognosis of Ph-like ALL (https://songxiaodan03.shinyapps.io/RFpredictionmodelforPHlikeALL/) could facilitate healthcare professionals in carrying out clinical evaluation.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1650810"},"PeriodicalIF":4.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sirtuin 6 mediates the therapeutic effect of endometrial regenerative cell-derived exosomes in alleviation of acute transplant rejection by weakening c-myc-dependent glutaminolysis.","authors":"Tong Liu, Chenglu Sun, Xu Liu, Pengyu Zhao, Bo Shao, Yini Xu, Yiyi Xiao, Hongda Wang, Qiang Chen, Guangmei Yang, Hao Wang","doi":"10.3389/fcell.2025.1564382","DOIUrl":"10.3389/fcell.2025.1564382","url":null,"abstract":"<p><strong>Background: </strong>Despite the rapid development of immunosuppressive drugs, acute rejection (AR) remains a cause of allograft dysfunction and allograft failure. Although endometrial regenerative cell-derived exosomes (ERC-Exos) effectively alleviate AR, more research is required to fully understand the underlying mechanisms. Thus, this study aimed to determine whether sirtuin 6 (SIRT6) mediates the therapeutic effect of ERC-Exos on AR and elucidate the underlying mechanisms.</p><p><strong>Methods: </strong>The expression of SIRT6 was verified in ERC-Exos by Western blot. ERC-Exos with extremely low expression of SIRT6 (SIRT6-KD-ERC-Exos) were obtained by transducing shRNA-SIRT6 in ERCs. C57BL/6 recipient mice were transplanted with heart grafts from BALB/c donor mice and divided into three groups: untreated, ERC-Exo-treated, and SIRT6-KD-ERC-Exo-treated groups. Recipient mice were sacrificed on post-operative day 8 for the determination of graft pathological changes, intra-graft immunocyte infiltration, splenic CD4⁺ T cell populations, and serum cytokine levels <i>in vivo</i>. The proportion of CD4⁺ T cells and their secreting cytokine levels were determined <i>in vitro</i>. Besides, the underlying mechanisms were also investigated <i>in vitro</i>.</p><p><strong>Results: </strong>ERC-Exos expressed SIRT6, and cardiac graft survival was increased by SIRT6-expressing ERC-Exos. Graft pathological damage, intra-graft CD4⁺ T cell infiltration, and intra-graft inflammatory (Th1 and Th17) cell infiltration decreased, and intra-graft and serum inflammatory cytokine (interferon (IFN)-γ and interleukin (IL)-17) levels decreased in the SIRT6-expressing ERC-Exo-treated mice. Furthermore, in the recipient mice, ERC-Exo treatment markedly increased the differentiation of regulatory T cells (Tregs) while significantly decreasing that of Th1 and Th17 cells. In a similar vein, ERC-Exo therapy raised the levels of the anti-inflammatory cytokine IL-10 <i>in vitro</i> while decreasing those of IFN-γ and IL-17. By suppressing the expression of important proteins linked to glutaminolysis and further deactivating the mammalian target of rapamycin complex 1 (mTORC1) pathway, ERC-Exos reduced the uptake and use of glutamine in naïve CD4⁺ T cells, according to mechanism exploration. In contrast, SIRT6-KD-ERC-Exos considerably reversed these trends and changes both <i>in vivo</i> and <i>in vitro</i>.</p><p><strong>Conclusion: </strong>SIRT6 is crucial in mediating ERC-Exos to remodel CD4⁺ T cell differentiation by weakening c-Myc-dependent glutaminolysis, thereby alleviating AR.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1564382"},"PeriodicalIF":4.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding congenital heart disease: a multi-omic framework for cardiac lineage and regulatory dysfunction.","authors":"Huasheng Lv, Fengyu Sun, You Chen","doi":"10.3389/fcell.2025.1659884","DOIUrl":"10.3389/fcell.2025.1659884","url":null,"abstract":"<p><p>Congenital heart disease (CHD) is the most prevalent birth defect worldwide, arising from disruptions in the tightly regulated processes of cardiac lineage specification and morphogenesis. Traditional models linking genotype to phenotype have been limited by low resolution and insufficient temporal mapping. Recent advances in single-cell RNA sequencing, spatial transcriptomics, and integrative multi-omics have transformed our understanding of CHD by enabling high-resolution analyses of the cellular origins and regulatory landscapes underlying malformations. This review synthesizes current insights into the developmental trajectories of first and second heart field progenitors, cardiac neural crest cells, and emerging progenitor populations. We highlight how combining genome-wide association studies with single-cell and spatial atlases can map non-coding risk variants to precise spatiotemporal cell states. Additionally, cardiac organoid and engineered developmental models provide innovative platforms for validating gene function and modeling lineage-specific defects in human tissues. Together, these technologies are shifting CHD research toward a mechanistic, cell-type-resolved framework, opening new avenues for precision diagnostics, targeted prevention, and regenerative therapies aimed at restoring normal cardiac development.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1659884"},"PeriodicalIF":4.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Eco-evo-devo: an emergent integrative discipline of biology.","authors":"Miguel Brun Usan, Rodrigo Nunes-da-Fonseca, Kathryn D Kavanagh, Jacqueline E Moustakas-Verho, Roland Zimm","doi":"10.3389/fcell.2025.1681036","DOIUrl":"https://doi.org/10.3389/fcell.2025.1681036","url":null,"abstract":"","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1681036"},"PeriodicalIF":4.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing therapeutic target discovery in pulmonary diseases: evolution and application of space exploration technologies.","authors":"Bo Yang, Quan Zheng, Guozheng Li, Bingnan Liao, Zhongxiao Lin, Hao He","doi":"10.3389/fcell.2025.1657720","DOIUrl":"10.3389/fcell.2025.1657720","url":null,"abstract":"<p><p>Epigenetic alterations are associated with various pulmonary diseases. In recent years, the concept of epigenetic inheritance influenced by spatial variations has garnered increasing attention. Alterations in three-dimensional (3D) chromatin architecture have been demonstrated to play a crucial role in regulating gene expression and influencing the pathogenesis and progression of lung-related diseases. Techniques such as high-throughput chromosome conformation capture (Hi-C) have emerged as powerful tools for detecting spatial chromatin conformational changes. In this review, we summarize key targets identified through Hi-C and related methodologies in the context of pulmonary diseases and explore their potential implications for epigenetic therapies.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1657720"},"PeriodicalIF":4.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: 7th international symposium on peripheral nerve regeneration: peripheral nerve regeneration - advances and new directions.","authors":"Rui Alvites, Óscar Darío García","doi":"10.3389/fcell.2025.1701185","DOIUrl":"https://doi.org/10.3389/fcell.2025.1701185","url":null,"abstract":"","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1701185"},"PeriodicalIF":4.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol metabolic reprogramming drives the onset of DLBCL and represents a promising therapeutic target.","authors":"Lili Zhou, Wei Cheng, Dan Luo, Zhida Peng, Jiaqi Mei, Qingqing Luo, Tiantian Yu, Ya Wang, Zhixiang Lei, Chunhong Huang, Nianlong Yan, Daya Luo, Li Yu","doi":"10.3389/fcell.2025.1585521","DOIUrl":"10.3389/fcell.2025.1585521","url":null,"abstract":"<p><strong>Background: </strong>Cholesterol is an essential molecule for tumor cell growth and proliferation, and dysregulated cholesterol metabolism has been widely implicated in cancer pathogenesis. However, the specific role and underlying molecular mechanisms of cholesterol metabolism alterations in diffuse large B-cell lymphoma (DLBCL) remain poorly understood.</p><p><strong>Methods: </strong>We retrospectively analyzed clinical data from 200 DLBCL patients and 185 healthy controls, focusing on lipid and lipoprotein levels, including triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), and apolipoprotein E (ApoE). Univariate and multivariate Cox proportional hazard models were used to evaluate the prognostic value of these markers, and Kaplan-Meier analysis assessed their associations with overall survival (OS). Bioinformatics analysis predicted associations between lipid markers and cholesterol metabolism. Cellular experiments further investigated the expression of cholesterol metabolism-related proteins and the effect of the cholesterol-depleting agent Methyl-β-cyclodextrin (MβCD) on DLBCL cells.</p><p><strong>Results: </strong>We confirmed significant alterations in metabolic markers (such as TC and ApoA1) between the healthy control group and patients, which were significantly associated with patient prognosis and overall OS. Bioinformatics analysis revealed a strong correlation between these markers and elevated CD36 expression. In addition, DLBCL cells exhibited increased expression of cholesterol uptake and synthesis proteins (CD36, SREBP2, and HMGCR) and decreased expression of efflux proteins (APOA1, NR1H2 and ABCG1), consistent with cholesterol metabolic reprogramming. Treatment with MβCD disrupted CD36 expression and cholesterol metabolism, leading to reduced DLBCL cell survival.</p><p><strong>Conclusion: </strong>These findings underscore the pivotal role of cholesterol metabolic reprogramming in DLBCL progression. CD36 and related metabolic markers represent promising therapeutic targets, opening novel avenues for the treatment of this malignancy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1585521"},"PeriodicalIF":4.6,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12484024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxygen concentration modulates HDAC1-Mediated regulation of osteogenic signaling pathways in dental pulp cells.","authors":"Ci Song, Ping Li, Lin Lin, Ge Cao, Zhao Liu, Fei Liu, Ling Peng, Jingxing Dai, Buling Wu, Ting Chen","doi":"10.3389/fcell.2025.1627763","DOIUrl":"10.3389/fcell.2025.1627763","url":null,"abstract":"<p><strong>Background: </strong>Dental pulp regeneration represents a critical frontier in translational dentistry, with dental pulp stem cells (DPSCs) demonstrating exceptional reparative potential through their multipotent differentiation capacity. While oxygen tension is known to influence cellular physiology, its regulatory mechanisms on DPSC osteo/odontogenic differentiation remain poorly understood.</p><p><strong>Methods: </strong>We established physiologically relevant oxygen gradients (3%, 5%, 21% O₂) to mimic developmental and pathological pulp microenvironments. Cellular proliferation and osteogenic capacity were assessed through flow cytometry, CCK-8 assays, and Live/Dead staining. Differentiation markers (RUNX2, OCN, ALP, DSPP) were quantified via qRT-PCR, immunoblotting, and enzymatic activity assays. Pharmacological inhibition studies using Oltipraz (HIF-1α inhibitor) and Valproic acid (HDAC inhibitor) elucidated pathway interactions. Publicly available transcriptomic datasets were analyzed to identify hypoxia-regulated pathways, and protein interactions were predicted using bioinformatics tools.</p><p><strong>Results: </strong>Moderate hypoxia (5% O₂) significantly enhanced DPSC proliferation (p < 0.05 vs. normoxia) and upregulated osteogenic markers at transcriptional (1.8-3.2 fold) and translational levels. Severe hypoxia (3% O₂) suppressed both proliferation (p < 0.01) and differentiation markers (0.4-0.7 fold). HIF-1α inhibition reversed 5% O₂-mediated osteogenic enhancement (p < 0.01), while HDAC1 blockade with Valproic acid rescued differentiation capacity under 3% O₂ (1.5-2.1 fold induction). Mechanistically, HDAC1 appeared to influence HIF-1α protein levels in an oxygen-dependent manner, and its inhibition affected pathways consistent with alterations in chromatin remodeling, influencing VEGFA-mediated osteogenic signaling.</p><p><strong>Conclusion: </strong>Our findings establish an oxygen-sensitive HDAC/HIF-1α regulatory axis governing DPSC fate determination. The biphasic response to hypoxia gradients suggests microenvironmental optimization strategies could enhance pulp regenerative outcomes. These insights provide mechanistic foundations for developing HDAC-targeted approaches in endodontic regeneration.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1627763"},"PeriodicalIF":4.6,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12485506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional Chinese medicine derived exosome-like nanovesicles in wound repair and skin regeneration.","authors":"Kang Wang, Zi-Ting Yang, Fei Wang, Yun-Qi Ma, Yong Qing, Zhen-Yu Zhang","doi":"10.3389/fcell.2025.1680757","DOIUrl":"10.3389/fcell.2025.1680757","url":null,"abstract":"<p><p>Skin injuries, including acute wounds, burns, and chronic ulcers, pose significant clinical challenges due to their potential to cause delayed healing and functional impairment. Exosome-like nanovesicles (ELNVs) derived from traditional Chinese medicinal (TCM) herbs have recently emerged as promising natural agents for skin repair and regeneration. These nanoscale vesicles combine the structural advantages of plant-derived delivery systems with the inherent pharmacological activities of TCM phytochemicals, offering dual roles as both bioactive agents and therapeutic carriers. Accumulating evidence indicates that TCM-derived ELNVs modulate key processes in wound healing, including inflammation resolution, fibroblast and keratinocyte activation, angiogenesis, and oxidative stress reduction. Moreover, certain vesicles have demonstrated potential in promoting hair follicle regeneration and protecting against photoaging, further highlighting their relevance in functional skin restoration. Compared with vesicles from common edible plants, TCM-ELNVs benefit from standardized cultivation, well-established traceable sourcing systems, and consistent phytochemical profiles, enhancing their suitability for therapeutic development. This review summarizes recent progress in the characterization, biological functions, and preclinical applications of TCM-derived ELNVs in cutaneous healing. Special attention is given to their mechanisms of action and their potential to serve as platforms for drug delivery and regenerative therapies. Overall, TCM-ELNVs represent a promising class of bioactive nanovesicles with broad translational potential in wound repair and skin regenerative medicine.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1680757"},"PeriodicalIF":4.6,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12484199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}