Epigenetics最新文献

{"title":"Environmental cues signal through circadian control of sarcomeric gene expression during cardiomyocyte hypertrophy.","authors":"Adrian Arrieta, Alexa Jennings, Pratiti Dasgupta, Natalie D Gehred, Tatiana Gromova, Erik Sandoval, Kunhua Song, Mansoureh Eghbali, Matthew A Fischer, Thomas M Vondriska","doi":"10.1080/15592294.2026.2694794","DOIUrl":"10.1080/15592294.2026.2694794","url":null,"abstract":"<p><p>Environmental disruption alters circadian clock gene expression, increasing the risk of adverse cardiac events and suggesting cardiomyocyte-specific circadian responses to external stimuli. Analyses of previously reported transcriptomic data revealed increased expression of Titin-cap (Tcap) in adult compared to embryonic myocytes and identified myosin light chain 2 (Myl2) as clock-controlled. Given cardiac sarcomeric roles of the encoded proteins, we hypothesized that extracellular cues driving postnatal cardiac maturation and hypertrophy influence time-of-day Tcap and Myl2 expression. Tcap induction was concomitant with neonatal myocyte binucleation, fetal gene suppression, and increased heart weight during the early phase of cardiac growth. Since norepinephrine stimulates β-adrenergic and α-adrenergic receptors, the latter driving clock-controlled transcriptional remodeling, phase‑response curves of the β‑adrenergic agonist isoproterenol (ISO) following α-adrenergic stimulation with phenylephrine (PE) were performed on neonatal rat ventricular myocytes (NRVM), revealing periodic myocyte hypertrophy and TCAP protein expression. PE entrenched ISO-mediated Tcap suppression, to which oscillatory Per2 and Myl2 transcription was impervious. Differential NRVM culture density revealed biomass-dependent changes in Per2 and Tcap transcription and hypertrophy timing. Hypoxia initiated myocyte atrophy and Bmal1-dependent Tcap transcription, reflected in decreased heart weight and increased Tcap expression in hypoxic neonatal rat hearts. Tcap depletion impaired Bmal1 and fetal hypertrophic gene expression, compromised hypoxia-mediated Myl2 transcriptional suppression, and aggravated hypoxia-induced atrophy. In summary, Tcap and Myl2 are circadian genes differentially influenced by environmental factors, including adrenergic stimulation, paracrine signaling, and O₂ tension during postnatal cardiac maturation. These findings have implications for the distinct regulation of myocyte growth and maturation, by external cues during the postnatal period.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2694794"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic control of transposable elements in brain and brain disorders.","authors":"Corinne Smith, Peter J Hamilton","doi":"10.1080/15592294.2026.2732514","DOIUrl":"10.1080/15592294.2026.2732514","url":null,"abstract":"<p><p>Once considered somewhere between inert ('junk DNA') and parasitic ('selfish genetic elements'), transposable elements (TEs) are increasingly appreciated as inseparable from the healthy functioning of eukaryotic genomes. The ubiquitous TE sequences that make up about half of the human genome are sources of the physical genetic material necessary for establishing distinct domains of chromatin architecture, generating non-coding RNAs (ncRNAs), expanding transcription factor regulatory networks, and providing <i>cis</i>-regulatory elements to enable complex gene expression patterns. Given the critical roles for TEs in core genomic functions, the circumstances in which TEs become dysregulated are increasingly being explored in the context of human disease. While most TEs are silenced by host-mediated epigenetic and transcriptional mechanisms, certain tissues and cell types are noted to experience considerable TE transcription. The brain and nervous tissues notably exhibit highly dynamic TE activity, both in response to experience and across the lifespan. Here, we review the current state of research into epigenetic regulation of and by TEs with a focus on the brain. We explore the intersection of epigenetics and TEs in brain cell types, with emphasis on DNA and histone methylation, ncRNAs and small RNAs, and the function of TE-regulating transcription factors. We explore how epigenetic mechanisms involved in brain TE regulation may become dysfunctional in the context of neurodevelopmental, neurodegenerative, and neuropsychiatric disorders. We present and synthesize the mounting evidence implicating the epigenetic control of brain TEs as an under-explored mechanism in these complex disorders.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2732514"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early characterization of pregnancy glycemic traits in gestational diabetes mellitus by plasma cell-free mRNA and non-coding RNA.","authors":"Songchang Chen, Yuwei Liu, Tingyu Yang, Zunmin Wan, Jinghua Sun, Xuanyou Zhou, Jiayi Li, Jiayi Huang, Lanlan Zhang, Sijia Guo, Yuxuan Kang, Fang Chen, Hefeng Huang, Chenming Xu, Wen-Jing Wang","doi":"10.1080/15592294.2025.2612399","DOIUrl":"10.1080/15592294.2025.2612399","url":null,"abstract":"<p><p>In recent years, the incidence of gestational diabetes mellitus (GDM) has been steadily increasing, posing risks to the long-term health of both mother and child. We aim to characterize blood glucose levels of pregnant women and predict the risk of GDM during early pregnancy through plasma cell-free mRNA and non-coding RNA (cfRNA). Here, we collected plasma samples from 108 pregnant women (54 with GDM and 54 controls) at around 16 weeks of gestation. Following high-throughput sequencing, we performed differentially abundant genes analysis and evaluated correlations between cfRNA profiles and blood glucose levels. Based on these findings, we developed a predictive model utilizing cf-mRNA and cf-lncRNA signatures. We found that ribosomal genes (<i>RPL/RPS</i>) are decreased in GDM, negatively correlated with 1hGlu and 2hGlu, and enriched in protein synthesis metabolic pathways. Additionally, placental-derived cfRNA contributed less to plasma in GDM, with placental-specific gene <i>IGF2</i> significantly negatively correlated with blood glucose. Furthermore, 35 blood glucose correlated-cfRNA genes accurately predict GDM, with area under the curve of 0.84 in internal testing and 0.73 in external validation cohort. Our study reveals significant alterations in protein metabolic pathways and placenta-derived RNAs in plasma cfRNA prior to GDM diagnosis.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2612399"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12893693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The epigenetic archaeology of human-dog companionship.","authors":"Jamshid Faraji, Gerlinde A S Metz","doi":"10.1080/15592294.2026.2676911","DOIUrl":"10.1080/15592294.2026.2676911","url":null,"abstract":"<p><p>Humans have coexisted with dogs for at least 20,000 years, yet the biological consequences of long-term human-dog co-residence remain poorly understood. We propose that sustained exposure to dogs may have contributed to context-dependent variation in human stress regulation, immune function, and socio-emotional neurobiology through environmentally responsive epigenetic mechanisms. Here, we define an <i>epigenetic imprint</i> as detectable differences in gene-regulatory marks, including DNA methylation at environmentally sensitive loci, consistent with developmental plasticity and early-life environmental calibration rather than germline inheritance. In this Commentary, we integrate evidence from genomics, neuroscience, microbiome research, evolutionary anthropology, and palaeoepigenetics to examine whether multispecies living environments may represent an under-recognised biological exposure shaping human regulatory biology. We further outline a framework to test whether archaeologically inferred dog co-residence is associated with epigenetic and regulatory signatures in ancient human populations while accounting for major ecological and demographic confounds. Overall, we argue that human-dog cohabitation provides a plausible and testable model for investigating how long-term social and ecological relationships may influence stress and immune regulation across populations.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2676911"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13203029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148013979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic regulation of vertebrate limb development: from field specification to tissue morphogenesis.","authors":"Claudia Monserrat Vallejo-De Lira, Claudio Iván Galván-Hernández, Jesús Chimal-Monroy, Jessica Cristina Marin-Llera","doi":"10.1080/15592294.2026.2695477","DOIUrl":"10.1080/15592294.2026.2695477","url":null,"abstract":"<p><p>Vertebrate limb development provides an excellent model for understanding how epigenetic mechanisms coordinate the integration of positional information and temporal signals to generate complex three-dimensional structures. An increasing body of evidence shows that chromatin-based mechanisms, including DNA methylation, histone modifications, and higher-order chromatin organization, define the competence of progenitor cells to respond to morphogenetic signals with spatial and temporal precision during limb development. This review explores how epigenetic mechanisms orchestrate and regulate the major phases of limb formation: from field specification and bud induction to morphogenesis, lineage differentiation, and programmed cell death. Here, we examine how chromatin remodeling, histone and DNA modifications, and enhancer - promoter interactions functionally converge with developmental signaling pathways to control gene expression programs that govern timing, positional identity, and cell fate decisions. Furthermore, this review highlights recent advances that link epigenetic landscapes with morphogenetic outcomes and discusses how comparative epigenomic approaches are reshaping our understanding of evolutionary diversification in limb morphology.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2695477"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13349005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aurora kinase a phosphorylates and stabilizes UHRF1 to maintain DNA methylation and prostate cancer cell survival.","authors":"Qin Xiang, Yuchong Peng, Yubing Ye, Xiong Li","doi":"10.1080/15592294.2026.2719245","DOIUrl":"10.1080/15592294.2026.2719245","url":null,"abstract":"<p><p>Aberrant DNA methylation is a hallmark of prostate cancer (PCa) and plays a critical role in sustaining the epigenetic silencing of tumor suppressor genes. However, how oncogenic signaling pathways interface with the DNA methylation machinery remains poorly understood. In this study, we identify AURKA as a key regulator of global DNA methylation in PCa cells. AURKA depletion markedly reduces genomic 5-methylcytosine (5mC) levels, indicating its essential role in DNA methylation maintenance. Mechanistically, AURKA directly interacts with UHRF1-a crucial epigenetic regulator that recruits DNMT1 to hemimethylated DNA, and phosphorylates it at Ser76, thereby enhancing UHRF1 protein stability. AURKA depletion accelerates UHRF1 degradation via the ubiquitin-proteasome pathway, whereas AURKA overexpression stabilizes UHRF1 by suppressing its polyubiquitination. The phospho-deficient UHRF1 S76A mutant exhibits reduced stability and increased polyubiquitination, confirming that phosphorylation at Ser76 is critical for AURKA-mediated UHRF1 stabilization. Functionally, disruption of the AURKA-UHRF1 axis de-represses <i>p16</i> and <i>p21</i> and significantly impairs PCa cell proliferation; these effects are contingent upon UHRF1 phosphorylation, as only wild-type UHRF1, not the phospho-deficient S76A mutant, can rescue the observed phenotypic impairments. Collectively, our study reveals a previously unrecognized AURKA-UHRF1 signaling axis that links kinase activity to epigenetic maintenance. By phosphorylating UHRF1 at Ser76 and stabilizing its protein, AURKA sustains global DNA methylation and promotes PCa cell proliferation. These findings provide novel mechanistic insights into PCa biology and suggest that targeting this pathway may offer a promising therapeutic strategy.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2719245"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13618847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149059490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal peripheral DNA methylation remodeling following ketamine-assisted psychotherapy in major depressive disorder.","authors":"Arghavan Nepton, Sonya C Faber, Zachary Kaminsky, Mario Nucci, Hesam Farahani, Monnica T Williams, Sergio R Perez Rosal","doi":"10.1080/15592294.2026.2731659","DOIUrl":"10.1080/15592294.2026.2731659","url":null,"abstract":"<p><p>Ketamine produces rapid antidepressant effects, but the molecular processes associated with their persistence remain poorly defined in humans. We examined longitudinal DNA methylation changes in 10 adults with major depressive disorder undergoing ketamine-assisted psychotherapy using two pre-treatment assessments (T1, T2) and one post-treatment assessment (T3). Participants received three sessions of intranasal racemic ketamine within a structured psychotherapy protocol. Buccal DNA methylation was measured using the Illumina MethylationEPIC v2.0 BeadChip. Depressive symptoms improved markedly following treatment, with mean Beck Depression Inventory-II scores declining from the severe to the mild range (<i>p</i> < .001). Of 802,595 CpG loci evaluated, 20,770 met the nominal T3-versus-T2 screening criterion. Sequential filtering for methylation-change magnitude and movement relative to pre-treatment fluctuation identified 962 retained CpG loci, including 517 retained gene-annotated loci. A supplementary linear mixed-effects analysis modeled repeated measurements within participants across the 603 preselected gene-annotated magnitude-filtered loci; because these loci were selected using the same contrast and cohort, this analysis was not treated as independent confirmation. Exploratory enrichment analysis of this 603-locus set identified NOTCH1-related Reactome terms driven by NOTCH1, DLL1, and ADAM17. Within the retained signature, multiple core and adjacent Notch-related components formed a coherent signaling module spanning ligand, receptor processing, transcriptional regulation, and pathway cross-talk. These findings identify a structured peripheral methylation signature associated with ketamine-assisted psychotherapy. They do not establish brain-specific pathway activation or causality, but provide a longitudinal basis for investigating regulatory adaptations accompanying clinical improvement.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2731659"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13679325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood transcriptomic associations of epigenetic age in adolescents.","authors":"Dennis Khodasevich, Anne K Bozack, Saher Daredia, Julianna Deardorff, Kim G Harley, Brenda Eskenazi, Weihong Guo, Nina Holland, Andres Cardenas","doi":"10.1080/15592294.2025.2503824","DOIUrl":"10.1080/15592294.2025.2503824","url":null,"abstract":"<p><p>Epigenetic aging in early life remains poorly characterized, and patterns of gene expression can provide biologically meaningful insights. Blood DNA methylation was measured using the Illumina EPICv1.0 array and RNA sequencing was performed in blood in 174 adolescent participants (age range: 14-15 years) from the CHAMACOS cohort. Thirteen widely used epigenetic clocks were calculated, and their associations with transcriptome-wide RNA expression were tested using the <i>limma-voom</i> pipeline. We found evidence for substantial shared associations with RNA expression between different epigenetic clocks, including differential expression of <i>MYO6</i> and <i>ZBTB38</i> across five clocks. The epiTOC2, principal component (PC) PhenoAge, Hannum, PedBE and PC Hannum clocks were associated with differential expression of the highest number of RNAs, exhibiting associations with 22, 8, 5, 3, and 2 transcripts respectively. Generally, biological clocks were associated with differential expression of more genes than chronological clocks, and PC clocks were associated with differential expression of more genes relative to their CpG-trained counterparts. A total of 17 associations in our study were replicated in an independent adult sample (age range: 40-54 years). Our findings support the biological relevance of epigenetic clocks in adolescents and provide direction for selection of epigenetic ageing biomarkers in adolescent research.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2503824"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12087650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of histone methyltransferases in therapeutic resistance of NSCLC.","authors":"Fuze Zhu, Xudong Yang, Yanlong Yang, Xinghe Tong, Jie Jia, Xingkun Gu, Yunping Zhao, Xiaobo Chen","doi":"10.1080/15592294.2025.2536786","DOIUrl":"10.1080/15592294.2025.2536786","url":null,"abstract":"<p><p>Conventional treatments, including chemotherapy, immunotherapy, targeted therapy and radiotherapy, are effective clinical strategies for non-small cell lung cancer (NSCLC) patients, which can significantly improve life quality and prolong survival time. However, the application of drugs in NSCLC patients inevitably leads to therapeutic resistance. In recent years, many studies have shown that histone methyltransferases (HMTs), including both protein arginine methyltransferases (PRMTs) and lysine methyltransferases (KMTs), play pivotal roles in tumor initiation, progression, and treatment resistance. This review synthesizes current insights into histone methylation dynamics driving therapeutic resistance, with a focus on key HMTs and their mechanisms. Additionally, we discuss the molecular mechanisms underlying histone methylation-mediated therapeutic resistance and potential therapeutic strategies targeting histone methylation for overcoming therapeutic resistance in NSCLC.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2536786"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>PIK3R1</i> and <i>G0S2</i> are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation.","authors":"Dagne Daskeviciute, Becky Sainty, Louise Chappell-Maor, Caitlin Bone, Sarah Russell, Isabel Iglesias-Platas, Philippe Arnaud, Ana Monteagudo-Sánchez, Maxim V C Greenberg, Keran Chen, Africa Manerao-Azua, Guiomar Perez de Nanclares, Jon Lartey, David Monk","doi":"10.1080/15592294.2025.2523191","DOIUrl":"10.1080/15592294.2025.2523191","url":null,"abstract":"<p><p>Genomic imprinting is the parent-of-origin specific monoallelic expression of genes that result from complex epigenetic interactions. It is often achieved by monoallelic 5-methylcytosine, resulting in the formation of differentially methylated regions (DMRs). These show a bias towards oocyte-derived methylation and survive reprogramming in the pre-implantation embryo. Imprinting is widespread in the human placenta. We have recently performed whole-genome screens for novel imprinted placenta-specific germline DMRs (gDMRs) by comparing methylomes of gametes, blastocysts and various somatic tissues, including placenta. We observe that, unlike conventional imprinting, for which methylation at gDMRs is observed in all tissues, placenta-specific imprinting is associated with transient gDMRs, present only in the pre-implantation embryo and extra-embryonic lineages. To expand the list of <i>bona fide</i> imprinted genes subject to placenta-specific imprinting, we reinvestigated our list of candidate loci and characterized two novel imprinted genes, <i>PIK3R1</i> and <i>G0S2</i>, both of which display polymorphic imprinting. Interrogation of placenta single-cell RNA-seq datasets, as well as cell-type methylation profiles, revealed complex cell-type specificity. We further interrogated their methylation and expression in placental samples from complicated pregnancies, but failed to identify differences between intrauterine growth restricted or pre-eclamptic samples and controls, suggesting they are not involved in these conditions.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2523191"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}