Epigenetics最新文献_第4页

Chromatin accessibility profiling of Treg cells in acute urticaria. 急性荨麻疹Treg细胞的染色质可及性分析。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-05-12 DOI: 10.1080/15592294.2025.2503126

Leilei Wen, Xiaojing Zhang, Qiaoshan Yang, Fusheng Zhou

{"title":"Chromatin accessibility profiling of Treg cells in acute urticaria.","authors":"Leilei Wen, Xiaojing Zhang, Qiaoshan Yang, Fusheng Zhou","doi":"10.1080/15592294.2025.2503126","DOIUrl":"10.1080/15592294.2025.2503126","url":null,"abstract":"Acute urticaria can be a presenting symptom of anaphylaxis characterized by transient red swellings or fulminant wheals, often accompanied by severe pruritus. Numerous studies have substantiated the important involvement of regulatory T cells (Tregs) in the occurrence of allergic diseases and autoimmune diseases. However, the role of Tregs in the pathogenesis of acute urticaria is unclear. In this study, we found that the frequency of Tregs in peripheral blood mononuclear cells (PBMCs) was decreased in patients with acute urticaria compared with normal controls by flow cytometry. Analysis of Assay for transposase-accessible chromatin with sequencing (ATAC-seq) data identified 28 differentially accessible regions comparing Tregs from healthy individuals and patients with acute urticaria, all showing increased chromatin accessibility in the Tregs from acute urticaria. IL-1b was highly expressed in sera of patients with acute urticaria and the level of IL-1b was moderately positively related to white blood cell count. The elevated expression of IL-1b may be due to the diminished immune-suppressive function following the decline of Tregs in this study. We found that IL1B gene expression was also significantly increased in the skin lesions of both chronic spontaneous urticaria and solar urticaria compared to healthy controls. IL1B might play a key role in the development of acute urticaria and IL1B could be a potential prognostic biomarker and therapeutic target in urticaria.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2503126"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978049","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-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

Research progress on the mechanism of tumor cell ferroptosis regulation by epigenetics. 肿瘤细胞铁下垂调控机制的表观遗传学研究进展。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-05-06 DOI: 10.1080/15592294.2025.2500949

Yuyang Xiao, Mengyang He, Xupeng Zhang, Meng Yang, Zhangchi Yuan, Shanhu Yao, Yuexiang Qin

{"title":"Research progress on the mechanism of tumor cell ferroptosis regulation by epigenetics.","authors":"Yuyang Xiao, Mengyang He, Xupeng Zhang, Meng Yang, Zhangchi Yuan, Shanhu Yao, Yuexiang Qin","doi":"10.1080/15592294.2025.2500949","DOIUrl":"https://doi.org/10.1080/15592294.2025.2500949","url":null,"abstract":"Cancer remains a significant barrier to human longevity and a leading cause of mortality worldwide. Despite advancements in cancer therapies, challenges such as cellular toxicity and drug resistance to chemotherapy persist. Regulated cell death (RCD), once regarded as a passive process, is now recognized as a programmed mechanism with distinct biochemical and morphological characteristics, thereby presenting new therapeutic opportunities. Ferroptosis, a novel form of RCD characterized by iron-dependent lipid peroxidation and unique mitochondrial damage, differs from apoptosis, autophagy, and necroptosis. It is driven by reactive oxygen species (ROS)-induced lipid peroxidation and is implicated in tumorigenesis, anti-tumor immunity, and resistance, particularly in tumors undergoing epithelial-mesenchymal transition. Moreover, ferroptosis is associated with ischemic organ damage, degenerative diseases, and aging, regulated by various cellular metabolic processes, including redox balance, iron metabolism, and amino acid, lipid, and glucose metabolism. This review focuses on the role of epigenetic factors in tumor ferroptosis, exploring their mechanisms and potential applications in cancer therapy. It synthesizes current knowledge to provide a comprehensive understanding of epigenetic regulation in tumor cell ferroptosis, offering insights for future research and clinical applications.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2500949"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12064064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959332","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

A novel lncRNA, Lnc21q22.11, suppresses gastric cancer growth by inhibiting MEK/ERK pathway. 一种新型lncRNA ln21q22.11通过抑制MEK/ERK通路抑制胃癌生长。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-06-02 DOI: 10.1080/15592294.2025.2512764

Cheng Zhu, Meiying Zhang, Weili Yang, Aiai Gao, Xiaoyuan Yu, Xiaomo Su, Runsheng Chen, Mingzhou Guo

{"title":"A novel lncRNA, Lnc21q22.11, suppresses gastric cancer growth by inhibiting MEK/ERK pathway.","authors":"Cheng Zhu, Meiying Zhang, Weili Yang, Aiai Gao, Xiaoyuan Yu, Xiaomo Su, Runsheng Chen, Mingzhou Guo","doi":"10.1080/15592294.2025.2512764","DOIUrl":"10.1080/15592294.2025.2512764","url":null,"abstract":"Gastric cancer (GC) is one of the most common malignancies with limited treatment options and poor prognosis. Therefore, it is necessary to identify new markers for the development of novel therapeutic strategies. Long non-coding RNAs (lncRNAs) have emerged as pivotal players in cancer. However, RNA-based cancer therapy has been challenged by non-specificity and adverse immune effects. Thus, a comprehensive understanding of the functional roles of lncRNAs and their regulatory networks in downstream pathways may provide more specific targets. In this study, we identified a novel lncRNA, Lnc21q22.11, encoded by the region of chromosome 21q22.11. The full-length transcript was 1202 nt, and its expression was reduced in GC. The expression of Lnc21q22.11 was regulated by histone methylation. Lnc21q22.11 inhibited GC cell proliferation, colony formation, invasion, and migration. Lnc21q22.11 suppressed N87 cell xenograft growth in mice. Mechanistically, Lnc21q22.11 inhibited the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) signaling pathway by interacting with MYH9 in GC cells. Loss of or reduced Lnc21q22.11 expression sensitized GC cells to MEK inhibitor. In conclusion, Lnc21q22.11 is a novel lncRNA in gastric cancer. It suppresses gastric cancer growth by inhibiting the MEK/ERK signaling pathway both in vitro and in vivo.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2512764"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208030","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. 在非裔巴西人群中，血压控制基因的差异甲基化与原发性高血压有关。

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

Adaptation and changing phenotypes through transgenerational epigenetics. 通过跨代表观遗传学适应和改变表型。

IF 3.2 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-08-13 DOI: 10.1080/15592294.2025.2460246

Lon J Van Winkle, Rebecca J Ryznar, Philip M Iannaccone

引用次数: 0

METTL14-mediated m⁶A modification of DDIT4 promotes its mRNA stability in aging-related idiopathic pulmonary fibrosis. mettl14介导的m6A修饰DDIT4促进其mRNA在衰老相关特发性肺纤维化中的稳定性。

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

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":"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. CircMYH9通过募集EIF4A3促进乳腺癌进展，从而促进SPAG6 mRNA的稳定性。

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

PRMT1 promotes immune escape in hepatocellular carcinoma by regulating arginine methylation modification of MYC protein. PRMT1通过调节MYC蛋白的精氨酸甲基化修饰促进肝细胞癌的免疫逃逸。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-05-22 DOI: 10.1080/15592294.2025.2509044

Han Zhou, Yang Wang, Dan Wang, Mei Zhang, Kaidi Wang, Chunhui Liu

{"title":"PRMT1 promotes immune escape in hepatocellular carcinoma by regulating arginine methylation modification of MYC protein.","authors":"Han Zhou, Yang Wang, Dan Wang, Mei Zhang, Kaidi Wang, Chunhui Liu","doi":"10.1080/15592294.2025.2509044","DOIUrl":"10.1080/15592294.2025.2509044","url":null,"abstract":"Arginine methyltransferase 1 (PRMT1) is widely recognized as an oncogene in various cancers. However, its specific role and underlying mechanisms in hepatocellular carcinoma (HCC) remain insufficiently understood. This study investigated the function of PRMT1 in HCC development and immune evasion. A comprehensive approach combining database analysis (including TCGA, The Human Protein Atlas, Kaplan-Meier Plotter, and TIMER2.0), molecular techniques (such as RT-qPCR, Western blot analysis, and co-immunoprecipitation), cell-based assays (including MTT, colony formation, transwell, and T cell killing assays), and in vivo models was employed to explore PRMT1's role in HCC. The findings revealed a marked upregulation of PRMT1 in both HCC clinical samples and cell lines. Depletion of PRMT1 inhibited cell proliferation and immune evasion while reducing cell migration and invasion. Mechanistically, PRMT1 was shown to interact with MYC, facilitating its arginine methylation and enhancing its protein stability. Moreover, re-expression of MYC significantly reversed the anti-tumour effects associated with PRMT1 depletion. In vivo experiments further corroborated these results. Collectively, PRMT1 promotes HCC progression and immune escape by mediating ADMA methylation of MYC, thereby regulating its stability and expression.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2509044"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119038","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