Epigenomics最新文献

{"title":"Beyond tissue biopsy: ctDNA methylation analysis for prediction of colorectal cancer prognosis.","authors":"Takahiro Irie, Kiichi Sugimoto","doi":"10.1080/17501911.2026.2719145","DOIUrl":"10.1080/17501911.2026.2719145","url":null,"abstract":"<p><p>Accurate prognostic stratification remains a major challenge in colorectal cancer (CRC), as substantial heterogeneity in clinical outcomes persists even within the same pathological stage. While mutation-based circulating tumor DNA (ctDNA) analysis has transformed postoperative risk assessment by enabling detection of molecular residual disease (MRD), it primarily reflects the presence of tumor-derived genetic alterations and may not fully capture the biological processes underlying tumor progression. DNA methylation represents a complementary molecular layer that reflects coordinated regulatory states associated with tumor behavior, including transcriptional programs and cellular plasticity. Recent studies suggest that ctDNA methylation profiling may provide additional prognostic information beyond conventional clinicopathological factors and mutation-based assays, particularly in early-stage and postoperative settings. However, important challenges remain, including assay heterogeneity, lack of standardized metrics, and the need for robust external validation. In this Perspective, we examine the limitations of current prognostic frameworks and discuss the potential role of ctDNA methylation analysis as part of an integrated, multidimensional model for risk stratification in CRC. We propose that incorporating epigenetic information may refine prognostic assessment, while emphasizing the need for rigorous validation prior to clinical implementation.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1127-1135"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide DNA methylation landscapes in gallbladder carcinoma: revealing shared and distinct epigenetic signatures across subtypes.","authors":"Devbrat Singh, Shubham Krushna Talware, Shridhar Mishra, Pallavi Srivastava, Sayali Mukherjee, Anshuman Pandey, Mohammad Imran Siddiqi, Vandana Tiwari, Nuzhat Husain","doi":"10.1080/17501911.2026.2730905","DOIUrl":"10.1080/17501911.2026.2730905","url":null,"abstract":"<p><strong>Background: </strong>Gallbladder cancer is an aggressive malignancy with poor survival rates, there are biologically distinct subtypes, yet genome-wide epigenetic differences remain poorly understood. This study was designed as an exploratory investigation of subtype-specific DNA methylation patterns.</p><p><strong>Methods: </strong>The study included sixteen gallbladder tissue sample (adenocarcinoma, <i>n</i> = 6; ICPN with invasion, <i>n</i> = 6; controls, <i>n</i> = 4). Genome-wide DNA methylation profiling was performed using the Illumina Infinium MethylationEPIC (850K) array. Differential methylation was assessed using Δβ ≥ 0.2 and FDR < 0.05, with emphasis on effect sizes. Chromosomal distribution, CpG island annotation, Gene Ontology enrichment, protein-protein interaction networks, and promoter-specific methylation patterns were examined.</p><p><strong>Results: </strong>GBC demonstrated predominant global hypomethylation, with adenocarcinoma showing marked promoter hypomethylation (79.2%), compared with ICPN (54.7%). Adenocarcinoma exhibited enrichment of transcriptional and proliferative pathways whereas ICPN showed stress-response, autophagy, and apoptotic pathway enrichment. A set of 543 consensus genes displayed recurrent methylation changes across all comparisons, suggesting shared epigenetic remodeling duringndisease progression.</p><p><strong>Conclusions: </strong>This exploratory study identifies distinct and shared epigenetic signatures across gallbladder carcinoma subtypes, highlighting subtype-specific promoter remodeling. These findings provide a foundation for future large-scale validation studies integrating methylation, transcriptomic, and clinical outcome.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1087-1099"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging regulators of human physiology and disease; sORF-encoded microproteins.","authors":"Ayman M Mustafa, Rebaz M Ali, Sami S Omar, Sanaa O Karim, Shvan H Mohammed, Hussein M Hamasalih, Shvan L Ezzat, Abdullah Dler Ahmad, Karukh K Mohammed, Fahmi H Kakamad","doi":"10.1080/17501911.2026.2715309","DOIUrl":"10.1080/17501911.2026.2715309","url":null,"abstract":"<p><p>The human genome contains hundreds of thousands of short open reading frames (sORFs), yet their translational products, hereafter referred to as sORF-encoded microproteins (also historically termed micropeptides), have long remained overlooked in conventional genome annotation. Increasing evidence demonstrates that these molecules play critical regulatory roles in human physiology and disease. This narrative review summarizes current knowledge regarding the classification, discovery, translational regulation, and biological significance of sORF-encoded microproteins. Their expression is tightly controlled by epigenetic mechanisms, including DNA methylation, Polycomb-mediated H3K27 trimethylation, and bivalent histone modifications, as well as epitranscriptomic regulation through N6-methyladenosine-mediated translation. Key microproteins such as Humanin, MOTS-c, Myoregulin, DWORF, HOXB-AS3-p, Mitoregulin, and CASIMO1 illustrate the diverse roles of sORF-derived peptides in cardiometabolic disease, neurodegeneration, and cancer. The review also highlights emerging therapeutic strategies, including epigenome editing, peptide replacement, and immunopeptidome-based neoantigen targeting. Collectively, the sORF-encoded microproteome represents an epigenetically integrated and functionally significant regulatory layer of the human proteome with major implications for fundamental biology and precision medicine.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1153-1173"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary impacts on the human methylome - focus on vitamin intake in context of health and disease risk.","authors":"Cristina Álvarez-Martín, Laila Evangelista, Yanyu Pan, J Alexander Beggs, Sylvia Zanesco, Rocío de la Iglesia, Elena Alonso-Aperte, Ricardo Costeira, Jordana T Bell","doi":"10.1080/17501911.2026.2705143","DOIUrl":"10.1080/17501911.2026.2705143","url":null,"abstract":"<p><p>Diet is a key modifiable component of health, and a major risk factor for chronic disease in humans. At the molecular level diet can affect DNA methylation (DNAm), an epigenetic process that is involved in gene expression regulation. Multiple studies have linked DNAm profiles to changes in diet across different layers. Specifically, intake of nutrients such as folate and vitamin B₁₂ has been associated with changes in human DNAm patterns genome-wide, linking dietary intakes to the potential modulation of gene activity. In this review we present a focused overview of recent findings from epigenome-wide association studies (EWAS) in human cohorts linking intake of specific vitamins to changes in the human methylome. We also discuss current gaps in knowledge and propose future directions to explore how exactly different components of diet influence the regulation of human gene function. One conclusion is the relative consistency of CpG-level DNAm signal replication in prenatal and early-life folate studies. In contrast, while biologically plausible, evidence from adult nutritional epigenome-wide association studies remains more heterogeneous. Ultimately, nutrition represents a powerful tool with the potential to support health and influence long-term biological processes through gene regulation, offering promising avenues for strategies aimed at disease prevention and healthy aging.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1137-1152"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A epitranscriptomic regulation in asthma: mechanisms and therapeutic prospects.","authors":"Wufei Ye, Jingrui Ye, Bohan Wang, Yang Ruan, Yanqiu Xu, Chaofeng Zhang","doi":"10.1080/17501911.2026.2721821","DOIUrl":"10.1080/17501911.2026.2721821","url":null,"abstract":"<p><p>Asthma is a heterogeneous airway disease in which chronic inflammation, epithelial barrier injury, immune-cell imbalance and airway remodeling interact to shape variable clinical phenotypes. N6-methyladenosine (m6A), the most abundant internal modification of eukaryotic mRNA, has emerged as a dynamic epitranscriptomic layer that regulates RNA splicing, export, stability, translation and decay. Recent profiling studies and mechanistic experiments indicate that m6A patterns and m6A regulators are altered in lung tissue, airway epithelial cells, airway smooth muscle cells and immune cells in asthma. These changes influence type 2 inflammation, the balance between T helper 1 (Th1) and T helper 2 (Th2) cells, the balance between T helper 17 (Th17) and regulatory T (Treg) cells, macrophage polarization, epithelial ferroptosis, ciliary function, mitochondrial stress, pollutant responses and structural remodeling. This Review synthesizes current evidence linking m6A writers, erasers and readers to asthma pathobiology, highlights context-dependent and sometimes opposing functions of key regulators such as METTL3, FTO and ALKBH5, and discusses how m6A signatures may inform biomarker discovery and therapeutic development. We also outline major translational barriers, including cell-type specificity, target validation, assay standardization and safety of pharmacologic m6A modulation.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1175-1187"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between DNA methylation-based aging clocks and periodontitis in aged adults: results from NHANES 1999-2002.","authors":"Yiyi Cai, Zhurong Cui, Yedan Shen, Lu Lin, Weijun Yu, Yue Shen, Bin Jiang, Eryi Lu, Min Jin","doi":"10.1080/17501911.2026.2732837","DOIUrl":"10.1080/17501911.2026.2732837","url":null,"abstract":"<p><strong>Background: </strong>DNA methylation aging clocks reflect biological aging, but their relationship with periodontitis has not been systematically evaluated. This study aimed to compare first- and second-generation DNA methylation clocks to identify the optimal epigenetic aging biomarker for periodontitis.</p><p><strong>Methods: </strong>We analyzed 1,559 adults (aged ≥50 years) from the NHANES database (1999-2002) using logistic regression, subgroup analysis, restricted cubic spline, and receiver operating characteristic analysis.</p><p><strong>Results: </strong>Higher quartiles of DNA methylation-based aging measures showed increased odds of periodontitis: PhenoAge (OR_quartile4vs1 = 2.507, 95% CI: 1.181-5.324) and GrimAge2 (OR_quartile4vs1 = 2.796, 95% CI: 1.093-7.154). Similar trends occurred for age acceleration measures, PhenoAgeAccel (OR_quartile4vs1 = 1.958, 95% CI: 1.039-3.689) and GrimAge2Accel (OR_quartile4vs1 = 2.667, 95% CI: 1.238-5.748). GrimAge2 demonstrated moderate discriminative ability (AUC = 0.700), which was the highest among the clocks assessed.</p><p><strong>Conclusion: </strong>Second-generation DNA methylation clocks, particularly PhenoAge and GrimAge2, were positively associated with periodontitis in older adults.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1113-1126"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A modular class-aware workflow for small RNA sequencing analysis using mouse sperm as a case study.","authors":"Da Lu, Huan Liao, Tishtar Daruwalla, Anthony J Hannan","doi":"10.1080/17501911.2026.2725425","DOIUrl":"10.1080/17501911.2026.2725425","url":null,"abstract":"<p><strong>Background: </strong>Small RNA sequencing analysis is challenging because RNA classes differ in biogenesis, sequence redundancy, genomic organization, and annotation reliability. Integrated workflows accommodating these constraints remain limited, particularly for fragment-level and cluster-level analysis.</p><p><strong>Methods: </strong>We present a reproducible, containerized, class-aware workflow for small RNA sequencing analysis, using mouse sperm as a case study. The workflow combines standardized preprocessing with complementary annotation and quantification strategies for microRNAs (miRNAs), transfer RNA-derived small RNAs (tsRNAs), ribosomal RNA-derived small RNAs (rsRNAs), and PIWI-interacting RNA (piRNA)-enriched genomic clusters. Using sperm small RNA data from offspring of lipopolysaccharide (LPS)-exposed male mice, we compared integrated-reference mapping, multi-class annotation, fragment-level tsRNA profiling, and genome-based piRNA cluster analysis, with custom modules for locus-aware harmonization and condition-specific cluster analysis.</p><p><strong>Results: </strong>Integrated-reference mapping aligned 88.17% of reads and retained 690 features after filtering. It identified 11 differentially expressed miRNAs between LPS and controls, while other classes showed limited signal. Fragment-level profiling improved tsRNA resolution. piRNA cluster analysis identified 958 control and 940 LPS clusters, with 18 control-specific and no LPS-specific clusters.</p><p><strong>Conclusion: </strong>This workflow supports transparent, reproducible, class-aware interpretation of small RNA sequencing data while emphasizing cautious interpretation of piRNA-enriched signals from total small RNA sequencing.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1071-1086"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the boundaries between epigenetics and religiosity/spirituality: a systematic review.","authors":"Angélica Salatino-Oliveira, Joana Carmona Neuwald Celeste, Carolina Moronte Sturmer, Matheus de Medeiros Padilha, Leandro Nascimento Silveira, Yuri Bandeira Rodrigues de Souza, Luís Henrique Toledo da Silva, Francielly Dias Pereira, Emanuel Burck Dos Santos, Marianna de Abreu Costa","doi":"10.1080/17501911.2026.2711569","DOIUrl":"10.1080/17501911.2026.2711569","url":null,"abstract":"<p><strong>Background: </strong>Associations between religiosity/spirituality (R/S) and health are well documented, but underlying mechanisms remain poorly understood. This review examined epigenetic and related molecular pathways that may underlie these associations.</p><p><strong>Methods: </strong>EMBASE, PubMed, Web of Science, and Scopus were searched through 8 January 2025. Eligible studies assessed at least one R/S variable, construct, or intervention and gene-expression-related outcomes, including DNA methylation (DNAm), histone modifications, microRNAs, noncoding RNAs, or protein-level changes. Results were narratively synthesized. Risk of bias was assessed using Joanna Briggs Institute tools.</p><p><strong>Results: </strong>Thirty-six studies were included, totaling 43,671 participants. Nineteen were cross-sectional, 22 were conducted in the United States, 23 involved community populations, and 10 included clinical samples. Overall, 39 instruments or measurement approaches assessed R/S. Outcomes included inflammatory, stress-related, lipid-related, and gene-regulatory markers, including C-reactive protein (CRP), interleukin-6, cortisol, lipid profile, DNAm, and messenger RNA. Findings were heterogeneous, with consistent inverse associations for CRP and a tendency toward lower cortisol with higher R/S, while other outcomes were mixed.</p><p><strong>Discussion: </strong>The evidence suggests a potential beneficial epigenetics influence of R/S. However, methodological weaknesses, heterogeneity, limited longitudinal evidence, and small samples limit interpretation. Future studies require prospective designs, standardized measures, large samples, and confounding control.</p><p><strong>Protocol registration: </strong>www.crd.york.ac.uk/prospero identifier is CRD42022327728.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"973-992"},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of TET function by PROSER1 in development and hematologic malignancies.","authors":"Xiang Li, Kasper D Rasmussen","doi":"10.1080/17501911.2026.2698006","DOIUrl":"10.1080/17501911.2026.2698006","url":null,"abstract":"<p><p>Ten eleven translocation (TET) proteins are central regulators of DNA methylation homeostasis and play essential roles in development and disease, including hematopoietic malignancies. Among the three TET family members, mutations in TET2 are frequently observed in hematologic disorders. TET enzymes catalyze the iterative oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and further oxidized derivatives, enabling DNA demethylation. Beyond catalysis, TET proteins also perform important non-enzymatic functions mediated through interactions with diverse protein partners, highlighting the importance of defining their regulatory interactome. Previous studies identified several TET-associated factors, including O-Linked N-acetylglucosamine transferase (OGT), members of the Drosophila behavior/human splicing (DBHS) protein family, and proline and serine-rich protein 1 (PROSER1). However, these interactions were largely considered independently. Recent findings now demonstrate that TET proteins, OGT, PROSER1, and DBHS proteins assemble into a higher-order regulatory unit termed the TOPD (TET-OGT-PROSER1-DBHS) complex. In this review, we discuss how TOPD provides a conceptual framework for understanding multicomponent regulation of TET function, spatial control of DNA demethylation, and maintenance of epigenetic homeostasis, with implications for developmental syndromes and hematopoiesis.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1011-1019"},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic modulators in triple-negative breast cancer: epigenetic modifications and future treatment perspectives.","authors":"Anita Choudhary, Pawan Kumar, Sohit Kashyap, Vishal Patidar, Anil Kumar, Anjana Munshi","doi":"10.1080/17501911.2026.2698002","DOIUrl":"10.1080/17501911.2026.2698002","url":null,"abstract":"<p><p>Triple Negative Breast Cancer (TNBC), an aggressive type of Breast Cancer (BC) characterized by the loss of expression of Estrogen Receptor (ER), Progesterone Receptor (PR), and Human Epidermal growth factor Receptor 2 (HER2) protein. TNBC is quite heterogenous in nature with limited available therapeutic options due to the lack of defined molecular targets. Epigenetic abnormalities have been implicated in the onset, progression, immune escape, and resistance to treatment in TNBC. Important epigenetic modulations, include DNA methylation, histone lactylation, histone modifications, and chromatin remodeling. Global hypomethylation contributes to genomic instability, while promoter hypermethylation inhibits tumor suppressor genes, by dysregulating their expression, thereby promoting uncontrolled proliferation, EMT, metastasis, and immune evasion in TNBC. Targeting epigenetic modulators, have the potential to develop novel therapeutic interventions have been developed and being explored. These epidrugs have proven to be effective in preclinical and clinical trials when used in combination with chemotherapy, immunotherapy, or targeted therapy, reducing drug resistance and aberrant proliferation. Despite of the advancements, challenges like target specificity, precise biomarkers and treatment related toxicity are the major hurdles. The review comprehensively summarized the important epigenetic alterations as well as novel treatment strategies with potential clinical applications in TNBC.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"993-1010"},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}