Epigenetics最新文献_第2页

DNA-based cell typing in menstrual effluent identifies cell type variation by sample collection method: toward noninvasive biomarker development for women's health. 基于dna的月经流出液细胞分型通过样本收集方法识别细胞类型变化：面向女性健康的无创生物标志物开发。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-01-18 DOI: 10.1080/15592294.2025.2453275

Irma M Vlasac, Hannah G Stolrow, Zaneta M Thayer, Brock C Christensen, Luisa Rivera

引用次数: 0

Glucocorticoid receptor epigenetic activity in the heart.

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-02-25 DOI: 10.1080/15592294.2025.2468113

Olukunle Akinborewa, Mattia Quattrocelli

{"title":"Glucocorticoid receptor epigenetic activity in the heart.","authors":"Olukunle Akinborewa, Mattia Quattrocelli","doi":"10.1080/15592294.2025.2468113","DOIUrl":"10.1080/15592294.2025.2468113","url":null,"abstract":"The glucocorticoid receptor (GR) is a critical nuclear receptor that regulates gene expression in diverse tissues, including the heart, where it plays a key role in maintaining cardiovascular health. GR signaling influences essential processes within cardiomyocytes, including hypertrophy, calcium handling, and metabolic balance, all of which are vital for proper cardiac function. Dysregulation of GR activity has been implicated in various cardiovascular diseases (CVDs), highlighting the potential of GR as a therapeutic target. Remarkably, recent insights into GR's epigenetic regulation and its interaction with circadian rhythms reveal opportunities to optimize therapeutic strategies by aligning glucocorticoid administration with circadian timing. In this review, we provide an overview of the glucocorticoid receptor's role in cardiac physiology, detailing its genomic and non-genomic pathways, interactions with epigenetic and circadian regulatory mechanisms, and implications for cardiovascular disease. By dissecting these molecular interactions, this review outlines the potential of epigenetically informed and circadian-timed interventions that could change the current paradigms of CVD treatments in favor of precise and effective therapies.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2468113"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499980","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}

引用次数: 0

Differential methylation in blood pressure control genes is associated to essential hypertension in African Brazilian populations.

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-03-27 DOI: 10.1080/15592294.2025.2477850

Camila Cristina Avila Martins, Mariana Maschietto, Lilian Kimura, Lucas Alvizi, Kelly Nunes, Vinícius Magalhães Borges, Ana Cristina Victorino Krepischi, Regina Célia Mingroni-Netto

{"title":"Differential methylation in blood pressure control genes is associated to essential hypertension in African Brazilian populations.","authors":"Camila Cristina Avila Martins, Mariana Maschietto, Lilian Kimura, Lucas Alvizi, Kelly Nunes, Vinícius Magalhães Borges, Ana Cristina Victorino Krepischi, Regina Célia Mingroni-Netto","doi":"10.1080/15592294.2025.2477850","DOIUrl":"10.1080/15592294.2025.2477850","url":null,"abstract":"While genetic studies have provided insights into essential hypertension (EH, defined by high blood pressure ≥140/90 mmHg), investigation through epigenetics may address gaps in understanding its heritability. This study focused on African Brazilian populations in Vale do Ribeira River region, due to their high hypertension prevalence. We aimed to determine if DNA methylation is linked to hypertension susceptibility, through a genome-wide evaluation of 80 peripheral blood samples from normotensive (39) and hypertensive (41) individuals, with Infinium Methylation EPIC BeadChip platform. Data were analyzed using ChAMP package and cross-referenced with information from databases such as EWAS Atlas, GWAS catalog, GeneCards, literature, and tools such as VarElect and EWAS Toolkit. The comparison between hypertensive and normotensive revealed 190 differentially methylated CpG positions (DMPs) and 46 differentially methylated regions (DMRs), both with p-value ≤0.05. Among the DMPs, 27 were found to have a plausible role in blood pressure. Among the DMRs, those mapped to ABAT, BLCAP, CERS3, EIF4E, FMN1, GABBR1, HLA-DQB2, HOXA5, IL5RA, KCNH2, MIR487B, MIR539, MIR886, MKRN3, NUDT12, PON3, RNF39, RWDD3, and TSHBS1 were highlighted because of their lowest p-values, current literature, and/or VarElect prioritization. Our findings suggest that differences in methylation contribute to the high susceptibility to essential hypertension in these populations.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2477850"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718218","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}

引用次数: 0

Timing of dietary effects on the epigenome and their potential protective effects against toxins. 饮食对表观基因组的影响时间及其对毒素的潜在保护作用。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-01-18 DOI: 10.1080/15592294.2025.2451495

Lynnea A Nicholls, Kendall A Zeile, London D Scotto, Rebecca J Ryznar

{"title":"Timing of dietary effects on the epigenome and their potential protective effects against toxins.","authors":"Lynnea A Nicholls, Kendall A Zeile, London D Scotto, Rebecca J Ryznar","doi":"10.1080/15592294.2025.2451495","DOIUrl":"https://doi.org/10.1080/15592294.2025.2451495","url":null,"abstract":"Exposure to toxins causes lasting damaging effects on the body. Numerous studies in humans and animals suggest that diet has the potential to modify the epigenome and these modifications can be inherited transgenerationally, but few studies investigate how diet can protect against negative effects of toxins. Potential evidence in the primary literature supports that caloric restriction, high-fat diets, high protein-to-carbohydrate ratios, and dietary supplementation protect against environmental toxins and strengthen these effects on their offspring's epigenome. Most notably, the timing when dietary interventions are given - during a parent's early development, pregnancy, and/or lifetime - result in similar transgenerational epigenetic durations. This implies the existence of multiple opportunities to strategically fortify the epigenome. This narrative review explores how to best utilize dietary modifications to modify the epigenome to protect future generations against negative health effects of persistent environmental toxins. Furthermore, by suggesting an ideal diet with specific micronutrients, macronutrients, and food groups, epigenetics can play a key role in the field of preventive medicine. Based on these findings, longitudinal research should be conducted to determine if a high protein, high-fat, and low-carbohydrate diet during a mother's puberty or pregnancy can epigenetically protect against alcohol, tobacco smoke, and air pollution across multiple generations.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2451495"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CircMYH9 promotes the mRNA stability of SPAG6 by recruiting EIF4A3 to facilitate the progression of breast cancer.

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-03-27 DOI: 10.1080/15592294.2025.2482382

Shanji Fan, Ying Cui, Yingjie Liu, Yuehua Li, Hong Huang, Zecheng Hu

{"title":"CircMYH9 promotes the mRNA stability of SPAG6 by recruiting EIF4A3 to facilitate the progression of breast cancer.","authors":"Shanji Fan, Ying Cui, Yingjie Liu, Yuehua Li, Hong Huang, Zecheng Hu","doi":"10.1080/15592294.2025.2482382","DOIUrl":"10.1080/15592294.2025.2482382","url":null,"abstract":"The incidence rate of breast cancer (BC) ranks first among female malignant tumors. Late-stage BC patients are at risk of death from distant metastasis. Circular RNAs (circRNAs) play an important function in cancer development. This study looked at the role of circMYH9 in BC. The nude mouse tumor-bearing experiment was used to verify the role of circMYH9 in regulating BC tumor growth in mice. Gene expression and protein amount were tested by qRT-PCR, western blot, and IHC. The pathological changes in tumor tissues were analyzed by HE staining. Cell viability, proliferation, migration, and invasion were assessed using CCK8, colony formation assay, wound healing assay, and Transwell assay, respectively. The interactions between circMYH9, SPAG6, and EIF4A3 were analyzed by RIP assay. CircMYH9 was significantly upregulated in BC, and its upregulated was related to poor prognosis. CircMYH9 silencing markedly impaired BC cell proliferation, migration, and invasion. Mechanistically, circMYH9 promoted the mRNA stability and expression of SPAG6 by recruiting EIF4A3. As expected, SPAG6 overexpression abrogated inhibition mediated by circMYH9 knockdown on BC cell malignant behaviors. In addition, circMYH9 knockdown inhibited PI3K/Akt signal pathway by increasing PTEN expression in BC cells, while was reversed by SPAG6 upregulation. PTEN inhibition abolished inhibition induced by circMYH9 downregulation on BC malignant progression. Moreover, circMYH9 silencing inhibited tumor growth in mice. CircMYH9 overexpression regulated the PTEN/PI3K/AKT pathway by increasing SPAG6 mRNA stability through recruiting EIF4A3, thereby promoting BC malignant progression.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2482382"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718213","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}

引用次数: 0

METTL14-mediated m⁶A modification of DDIT4 promotes its mRNA stability in aging-related idiopathic pulmonary fibrosis.

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-02-07 DOI: 10.1080/15592294.2025.2462898

Dan Li, Li Qian, Yufeng Du, Lifang Liu, Ziyue Sun, Yongkang Han, Xiangrui Guo, Chao Shen, Zheng Zhang, Xuejun Liu

{"title":"METTL14-mediated m6A modification of DDIT4 promotes its mRNA stability in aging-related idiopathic pulmonary fibrosis.","authors":"Dan Li, Li Qian, Yufeng Du, Lifang Liu, Ziyue Sun, Yongkang Han, Xiangrui Guo, Chao Shen, Zheng Zhang, Xuejun Liu","doi":"10.1080/15592294.2025.2462898","DOIUrl":"10.1080/15592294.2025.2462898","url":null,"abstract":"Although N6-methyladenosine (m6A) may be related to the pathogenesis of fibrotic process, the mechanism of m6A modification in aging-related idiopathic pulmonary fibrosis (IPF) remains unclear. Three-milliliter venous blood was collected from IPF patients and healthy controls. MeRIP-seq and RNA-seq were utilized to investigate differential m6A modification. The expressions of identified m6A regulator and target gene were validated using MeRIP-qPCR and real-time PCR. Moreover, we established an animal model and a senescent model of A549 cells to explore the associated molecular mechanism. Our study provided a panorama of m6A methylation in IPF. Increased peaks (3756) and decreased peaks (4712) were observed in the IPF group. The association analysis showed that 749 DEGs were affected by m6A methylation in IPF. Among the m6A regulators, the expression of METTL14 decreased in IPF. The m6A level of our interested gene DDIT4 decreased significantly, but the mRNA level of DDIT4 was higher in IPF. This was further verified in bleomycin-induced pulmonary fibrosis. At the cellular level, it was further confirmed that METTL14 and DDIT4 might participate in the senescence of alveolar epithelial cells. The downregulation of METTL14 might inhibit the decay of DDIT4 mRNA by reducing the m6A modification level of DDIT4 mRNA, leading to high expression of DDIT4 mRNA and protein. Our study provided a panorama of m6A alterations in IPF and discovered METTL14 as a potential intervention target for epigenetic modification in IPF. These results pave the way for future investigations regarding m6A modifications in aging-related IPF.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2462898"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11810098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364170","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}

引用次数: 0

Deciphering the interplay between SETD2 mediated H3K36me3 and RNA N6-methyladenosine in clear cell renal cell carcinoma (ccRCC).

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-01-28 DOI: 10.1080/15592294.2025.2456418

Shafiq Shaikh, Xia Zhao, Ryan T Wagner, Xiaoyu Pan, Ryan A Hlady, Liguo Wang, Thai H Ho, Keith D Robertson

{"title":"Deciphering the interplay between SETD2 mediated H3K36me3 and RNA N6-methyladenosine in clear cell renal cell carcinoma (ccRCC).","authors":"Shafiq Shaikh, Xia Zhao, Ryan T Wagner, Xiaoyu Pan, Ryan A Hlady, Liguo Wang, Thai H Ho, Keith D Robertson","doi":"10.1080/15592294.2025.2456418","DOIUrl":"10.1080/15592294.2025.2456418","url":null,"abstract":"RNA N6-methyladenosine (m6A) plays diverse roles in RNA metabolism and its deregulation contributes to tumor initiation and progression. Clear cell renal cell carcinoma (ccRCC) is characterized by near ubiquitous loss of VHL followed by mutations in epigenetic regulators PBRM1, SETD2, and BAP1. Mutations in SETD2, a histone H3 lysine 36 trimethylase (H3K36me3), are associated with reduced survival, greater metastatic propensity, and metabolic reprogramming. While m6A and H3K36me3 deregulation are separately implicated in renal tumorigenesis, H3K36me3 may participate directly in m6A targeting, but the m6A-H3K36me3 interplay has not been investigated in the context of ccRCC. Using RCC-relevant SETD2 isogenic knockout and rescue cell line models, we demonstrate a dynamic redistribution of m6A in the SETD2 depleted transcriptome, with a subset of transcripts involved in metabolic reprogramming demonstrating SETD2 dependent m6A and expression level changes. Using a panel of six histone modifications we show that m6A redistributes to regions enriched in gained active enhancers upon SETD2 inactivation. Finally, we demonstrate a reversal of transcriptomic programs involved in SETD2 loss mediated metabolic reprogramming, and reduced cell viability through pharmacologic inhibition or genetic ablation of m6A writer METTL3 specific to SETD2 deficient cells. Thus, targeting m6A may represent a novel therapeutic vulnerability in SETD2 mutant ccRCC.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2456418"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058016","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}

引用次数: 0

TET-mediated 5hmC in breast cancer: mechanism and clinical potential.

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-02-27 DOI: 10.1080/15592294.2025.2473250

Jiahang Zhang, Nadire Aishan, Zhongqiu Zheng, Siwei Ju, Qina He, Qingna Meng, Xixi Lin, Jiaheng Lang, Jichun Zhou, Yongxia Chen, Bojian Xie, Yangjun Cai, Feiyang Ji, Linbo Wang

引用次数: 0

Comprehensive analysis of eccDNA characteristics and associated genes expression in peripheral blood of ASLE and ISLE patients.

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-03-20 DOI: 10.1080/15592294.2025.2477903

Yali Peng, Huihui Tao, Dongzhou Liu, Donger Tang, Chunmei Wen, Mengyao Wu, Tiantian Xu, Guoying Wang, Xuejia Zheng, Yong Dai

{"title":"Comprehensive analysis of eccDNA characteristics and associated genes expression in peripheral blood of ASLE and ISLE patients.","authors":"Yali Peng, Huihui Tao, Dongzhou Liu, Donger Tang, Chunmei Wen, Mengyao Wu, Tiantian Xu, Guoying Wang, Xuejia Zheng, Yong Dai","doi":"10.1080/15592294.2025.2477903","DOIUrl":"10.1080/15592294.2025.2477903","url":null,"abstract":"To explore SLE staging markers, we analyzed eccDNA in plasma using circular sequencing, comparing healthy controls (HC), active SLE (ASLE), and inactive SLE (ISLE) patients. We found higher eccDNA levels and lower GC content in ASLE and ISLE compared to healthy controls, with a negative correlation between GC content and anti-daDNA, C3, and C4 levels in SLE and HC samples. Differential expression of exon-derived eccGenes in ASLE and ISLE suggests their role in SLE development, with KEGG analysis showing enrichment in SLE-related pathways for these differentially expressed genes. By protein-protein interactions network analysis we found 9 exon-derived eccGenes that were significantly differentially expressed and scored high in both ISLE-HC and ASLE-ISLE as diagnostic criteria for differentiating different disease stages of SLE. In conclusion, the present study reveals that eccDNA length GC content as well as chromosomal distribution in ASLE, ISLE and HC suggests that with eccDNA is associated with the creation of SLE, suggesting GC count of eccDNA as a diagnostic marker for systemic lupus erythematosus. Significant changes in the abundance of eccDNA-related genes from exons such as SOS1, GAD2, BCL11B, PPT1, and GCNT3 were observed in ISLE as compared to ASLE and HC groups and were significantly correlated with SLEDAI-2K. This suggests that these exon-derived eccGenes may play a role in the development and progression of the disease. Consequently, the abundance levels of these exon-derived eccGenes could potentially assist in distinguishing different stages of SLE, beyond a confirmed diagnosis, thus serving as possible biomarkers for the condition.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2477903"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662872","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}

引用次数: 0

DNA methylation heterogeneity attributable to a complex tumor immune microenvironment prompts prognostic risk in glioma. 复杂的肿瘤免疫微环境导致的DNA甲基化异质性提示胶质瘤的预后风险。

IF 3.7 3区生物学

Epigenetics Pub Date : 2024-12-01 Epub Date: 2024-03-05 DOI: 10.1080/15592294.2024.2318506

Shuangyue Ma, Xu Pan, Jing Gan, Xiaxin Guo, Jiaheng He, Haoyu Hu, Yuncong Wang, Shangwei Ning, Hui Zhi

{"title":"DNA methylation heterogeneity attributable to a complex tumor immune microenvironment prompts prognostic risk in glioma.","authors":"Shuangyue Ma, Xu Pan, Jing Gan, Xiaxin Guo, Jiaheng He, Haoyu Hu, Yuncong Wang, Shangwei Ning, Hui Zhi","doi":"10.1080/15592294.2024.2318506","DOIUrl":"10.1080/15592294.2024.2318506","url":null,"abstract":"Gliomas are malignant tumours of the human nervous system with different World Health Organization (WHO) classifications, glioblastoma (GBM) with higher grade and are more malignant than lower-grade glioma (LGG). To dissect how the DNA methylation heterogeneity in gliomas is influenced by the complex cellular composition of the tumour immune microenvironment, we first compared the DNA methylation profiles of purified human immune cells and bulk glioma tissue, stratifying three tumour immune microenvironmental subtypes for GBM and LGG samples from The Cancer Genome Atlas (TCGA). We found that more intermediate methylation sites were enriched in glioma tumour tissues, and used the Proportion of sites with Intermediate Methylation (PIM) to compare intertumoral DNA methylation heterogeneity. A larger PIM score reflected stronger DNA methylation heterogeneity. Enhanced DNA methylation heterogeneity was associated with stronger immune cell infiltration, better survival rates, and slower tumour progression in glioma patients. We then created a Cell-type-associated DNA Methylation Heterogeneity Contribution (CMHC) score to explore the impact of different immune cell types on heterogeneous CpG site (CpGct) in glioma tissues. We identified eight prognosis-related CpGct to construct a risk score: the Cell-type-associated DNA Methylation Heterogeneity Risk (CMHR) score. CMHR was positively correlated with cytotoxic T-lymphocyte infiltration (CTL), and showed better predictive performance for IDH status (AUC = 0.96) and glioma histological phenotype (AUC = 0.81). Furthermore, DNA methylation alterations of eight CpGct might be related to drug treatments of gliomas. In conclusion, we indicated that DNA methylation heterogeneity is associated with a complex tumour immune microenvironment, glioma phenotype, and patient's prognosis.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"19 1","pages":"2318506"},"PeriodicalIF":3.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027750","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}

引用次数: 0