EpigenomicsPub Date : 2026-02-01Epub Date: 2026-03-02DOI: 10.1080/17501911.2026.2633977
Jorge Hallak, Thiago Afonso Teixeira, João Pedro M Gismondi, Eduardo Zinoni S Pato, Robert John Aitken, Fabio Firmbach Pasqualotto, Sandro C Esteves
{"title":"Assessing the epigenetic consequences of ART in male infertility: what risks to embryo and offspring health?","authors":"Jorge Hallak, Thiago Afonso Teixeira, João Pedro M Gismondi, Eduardo Zinoni S Pato, Robert John Aitken, Fabio Firmbach Pasqualotto, Sandro C Esteves","doi":"10.1080/17501911.2026.2633977","DOIUrl":"10.1080/17501911.2026.2633977","url":null,"abstract":"<p><p>Male infertility affects approximately 7 to 8% of men worldwide and is influenced by both genetic and epigenetic factors. Epigenetic mechanisms - including DNA methylation, histone modifications, and non-coding RNAs - are essential for spermatogenesis, sperm function, and early embryonic development. Disruptions in these processes can impair fertility and embryo viability. Assisted reproductive technologies (ART), particularly intracytoplasmic sperm injection (ICSI), have enabled conception in previously untreatable cases; however, by bypassing natural selection barriers, they may facilitate the transmission of epigenetic abnormalities. This narrative review summarizes recent clinical and experimental evidence on sperm epigenetics, emphasizing paternal health, sperm epigenetic signatures, and ART-associated developmental risks. During spermatogenesis, extensive epigenetic remodeling occurs, including protamine-histone exchange, selective histone retention, and RNA packaging, all critical for embryogenesis. Conditions such as varicocele, obesity, advanced paternal age, toxin exposure, and malignancy have been linked to abnormal DNA methylation, altered chromatin structure, and dysregulated small RNAs. Seminal extracellular vesicles also mediate environmental influences on implantation and immune modulation. Because ART coincides with windows of epigenetic vulnerability, laboratory procedures - including sperm selection, cryopreservation, and embryo culture - may contribute to imprinting disturbances. Understanding these mechanisms is essential to optimize reproductive safety while preserving ART efficacy.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"255-267"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147325046","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}
EpigenomicsPub Date : 2026-02-01Epub Date: 2026-01-24DOI: 10.1080/17501911.2026.2617179
Ana Claudia Rossini Venturini, Caroline Fogagnolo, Gabriela Ueta Ortiz, Guilherme da Silva Rodrigues, Arthur Polveiro da Silva, Natália Yumi Noronha, Gabriela Ferreira Abud, Bianca Monteiro Silva, Gabriela Geraldo Benzoni, Marcela Augusta de Souza Pinhel, Lígia Moriguchi Watanabe, Chanachai Sae-Lee, Sofia Germano Travieso, Marcela Coffacci de Lima Viliod, Carla Barbosa Nonino, Adelino Sanchez Ramos da Silva, Ellen Cristini de Freitas
{"title":"Accelerated epigenetic aging and shorter DNA methylation-based telomere length in sarcopenic obesity: an exploratory pilot study.","authors":"Ana Claudia Rossini Venturini, Caroline Fogagnolo, Gabriela Ueta Ortiz, Guilherme da Silva Rodrigues, Arthur Polveiro da Silva, Natália Yumi Noronha, Gabriela Ferreira Abud, Bianca Monteiro Silva, Gabriela Geraldo Benzoni, Marcela Augusta de Souza Pinhel, Lígia Moriguchi Watanabe, Chanachai Sae-Lee, Sofia Germano Travieso, Marcela Coffacci de Lima Viliod, Carla Barbosa Nonino, Adelino Sanchez Ramos da Silva, Ellen Cristini de Freitas","doi":"10.1080/17501911.2026.2617179","DOIUrl":"10.1080/17501911.2026.2617179","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenic obesity (SO), defined as the coexistence of excess fat mass and low muscle mass/function, has been linked to adverse outcomes. Epigenetic alterations are central hallmarks of aging. Evaluating how obesity, sarcopenia, and SO are related to epigenetic aging biomarkers may provide insights into cellular aging and disease risk.</p><p><strong>Methods: </strong>In this cross-sectional study, 30 older women were classified into the control, obesity, sarcopenia, and SO groups and underwent anthropometry measurements, body composition analysis, and handgrip strength. Blood DNA methylation (DNAm) biomarkers were used to estimate eight epigenetic clocks (Horvath, Hannum, DNAmTL, PhenoAge, GrimAge, GrimAge2, Zhang, and FitAge) and to calculate intrinsic and extrinsic epigenetic age acceleration (IEAA and EEAA). Associations were tested with Bayesian linear and quantile regressions, adjusted for age and HOMA-IR.</p><p><strong>Results: </strong>SO was associated with higher EEAA, DNAmFitAge, and Hannum clock estimates, and shorter DNAmTL in both models. Obesity showed positive associations with these clocks in adjusted models and higher quantiles.</p><p><strong>Conclusions: </strong>SO is associated with accelerated aging and shorter DNAmTL. Obesity contributes to biological aging, whereas sarcopenia without obesity does not. These findings suggest that excess adiposity combined with low muscle mass may worsen age-related decline, although the small sample size should be considered.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"169-183"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146040608","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}
EpigenomicsPub Date : 2026-02-01Epub Date: 2026-01-26DOI: 10.1080/17501911.2026.2617186
Xiaopeng Zheng, Chengru Yang, Deqiang Bian, Guoxin Shi, Li Wang, Xiaohan Li, Yufei Chen, Hua Xin, Liming Wang
{"title":"E2F1-driven cholesterol synthesis via the SND1/ACLY axis potentiates malignant progression in prostate cancer.","authors":"Xiaopeng Zheng, Chengru Yang, Deqiang Bian, Guoxin Shi, Li Wang, Xiaohan Li, Yufei Chen, Hua Xin, Liming Wang","doi":"10.1080/17501911.2026.2617186","DOIUrl":"10.1080/17501911.2026.2617186","url":null,"abstract":"<p><strong>Aim: </strong>This study aimed to clarify the mechanisms of E2F transcription factor 1 (E2F1) in the Cholesterol (CHOL) synthesis of Prostate cancer (PCa).</p><p><strong>Methods: </strong>CHOL component content was detected using a commercial test kit. The interaction between E2F1 and staphylococcal nuclease domain-containing protein 1 (SND1) promoter was confirmed employing dual luciferase and chromatin immunoprecipitation assay. RNA immunoprecipitation and RNA pull-down analysis were utilized to validate the interaction between SND1 and ATP citrate lyase (ACLY) mRNA. A xenograft tumor model was used to confirm these mechanisms in vivo.</p><p><strong>Results: </strong>E2F1, SND1, ACLY protein levels, along with CHOL concentrations, were up-regulated in human PCa tumor tissues. E2F1 enhanced cell proliferation, invasion, and CHOL synthesis in PCa cells. E2F1 could transcriptionally activate SND1, which subsequently bound to ACLY mRNA, stabilizing its expression. E2F1 induced CHOL synthesis via the enhancement of SND1/ACLY axis. E2F1 promoted CHOL synthesis and PCa tumor growth <i>in</i> <i>vivo</i>.</p><p><strong>Conclusion: </strong>E2F1 enhanced cell proliferation, invasion, and tumor growth by enhancing CHOL synthesis via the SND1/ACLY axis in PCa models.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"155-168"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050768","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}
EpigenomicsPub Date : 2026-02-01Epub Date: 2026-02-03DOI: 10.1080/17501911.2026.2623931
Paulina Plewa, Maciej Ćmil, Anna Jędrasiak, Jan Zadworny, Andrzej Pawlik
{"title":"The role of long non-coding RNA in the pathogenesis of aneurysms.","authors":"Paulina Plewa, Maciej Ćmil, Anna Jędrasiak, Jan Zadworny, Andrzej Pawlik","doi":"10.1080/17501911.2026.2623931","DOIUrl":"10.1080/17501911.2026.2623931","url":null,"abstract":"<p><p>Aneurysms are serious vascular conditions characterized by persistent dilatation of the blood vessel lumen, which can lead to rupture and become life-threatening. Their pathogenesis is complex and involves multiple biological mechanisms, including extracellular matrix degradation, oxidative stress, inflammation, and apoptosis of vascular smooth muscle cells. Long non-coding RNAs (lncRNAs), typically exceeding 200 nucleotides, perform numerous regulatory functions, including modulation of gene expression at the epigenetic, transcriptional, and post-transcriptional levels. Under pathological conditions, lncRNA expression can be markedly altered. A growing body of evidence indicates that lncRNAs play a key role in regulating cellular processes such as inflammation, apoptosis, and vascular remodeling, all of which are crucial to aneurysm development and progression. This review summarizes current knowledge on the involvement of lncRNAs in aneurysm pathophysiology and highlights recent research on their impact on vascular wall degradation, inflammatory responses, and smooth muscle cell survival. A literature review was conducted through a systematic search of PubMed, Scopus, and Web of Science using keywords related to lncRNAs and biological processes relevant to aneurysm development.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"231-242"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112666","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}
EpigenomicsPub Date : 2026-02-01Epub Date: 2026-01-31DOI: 10.1080/17501911.2026.2621199
Thao Griffith, George E Chlipala, Ashley Ford, Stefan J Green, Rosemary White-Traut, Sachin Amin, Lindsey Young, Caitlin Carlson, Linda Janusek
{"title":"Epigenetic investigation into <i>NR3C1</i> exon 1F and <i>HSD11B2</i>: associations with neurodevelopment and oral feeding skills in preterm infants.","authors":"Thao Griffith, George E Chlipala, Ashley Ford, Stefan J Green, Rosemary White-Traut, Sachin Amin, Lindsey Young, Caitlin Carlson, Linda Janusek","doi":"10.1080/17501911.2026.2621199","DOIUrl":"10.1080/17501911.2026.2621199","url":null,"abstract":"<p><strong>Aims: </strong>To examine the relationship between DNA methylation of <i>NR3C1</i> exon 1F and <i>HSD11B2</i> promoters and neurodevelopment, and oral feeding skills in preterm infants.</p><p><strong>Design: </strong>A longitudinal prospective cohort study was conducted.</p><p><strong>Methods: </strong>Data from 61 preterm infants who were born between 26 to 34 weeks gestational age without major comorbidities were analyzed. DNA methylation was evaluated from buccal samples. Neurodevelopment and oral feeding skills were evaluated using the Neurobehavioral Assessment of the Preterm Infants and the Early Feeding Skills Assessment, respectively.</p><p><strong>Results: </strong>Increased methylation at specific cytosine-guanine (CpG) dinucleotide sites within <i>NR3C1</i> exon 1F and <i>HSD11B2</i> promoters was associated with suboptimal neurodevelopmental and oral feeding outcomes, potentially reflecting heightened sensitivity to early life stress in the NICU. Conversely, certain methylation changes appear to be adaptive, promoting consistent suck-breathe coordination, or optimal behavioral and cardiorespiratory stability during oral feeding.</p><p><strong>Conclusion: </strong>The study highlights the complex relationship between DNA methylation of <i>NR3C1</i> exon 1F and <i>HSD11B2</i> promoters and neurodevelopment, and oral feeding skills in preterm infants.</p><p><strong>Implications for the profession and/or patient care: </strong>Findings emphasize the need for continued research into epigenetic mechanisms underlying neonatal adaptation and stress regulation, with potential implications for targeted epigenetic interventions to support optimal neurodevelopment and oral feeding skills.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"185-196"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12937114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092373","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}
EpigenomicsPub Date : 2026-02-01DOI: 10.1080/17501911.2026.2624361
Qi-Wei Liu, Zi-Qin Liu, Ming Wang, Yi-Jun Qi
{"title":"MicroRNAs in esophageal squamous cell carcinoma.","authors":"Qi-Wei Liu, Zi-Qin Liu, Ming Wang, Yi-Jun Qi","doi":"10.1080/17501911.2026.2624361","DOIUrl":"10.1080/17501911.2026.2624361","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy requiring improved early diagnosis and prognostic assessment. MicroRNAs (miRNAs), small non-coding RNAs that regulate gene expression, have emerged as promising biomarkers for ESCC. We conducted a comprehensive literature search in PubMed for studies published up to 2025. While miRNA profiles in ESCC tissues show significant associations with lymphatic dissemination, tumor progression, and patient survival, clinical translation remains limited by issues of sensitivity, specificity, and standardization. This review summarizes current knowledge on miRNA expression in ESCC, focusing on lymphatic dissemination and prognostic implications. We also explore circulating miRNAs as minimally invasive tools for early detection and treatment monitoring. By integrating recent findings, this article provides a critical overview of miRNA-based biomarkers to improve early diagnostic accuracy and therapeutic decision-making in ESCC.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"243-253"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099730","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":"Mitochondrial D-loop region methylation differentiates Parkinson's disease from atypical parkinsonism and Parkinson's disease dementia.","authors":"Bilge Karacicek, Bilgesu Ozturk, Ozgur Oztop Cakmak, Fatos Sibel Ertan, Pembe Keskinoglu, Sermin Genc","doi":"10.1080/17501911.2026.2627263","DOIUrl":"10.1080/17501911.2026.2627263","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss and α-synuclein aggregation. Epigenetic mechanisms, including mitochondrial DNA (mtDNA) methylation, have been implicated in PD pathogenesis. Methylation of the mitochondrial displacement loop (D-loop) region may play a role in neurodegenerative processes.</p><p><strong>Research design and methods: </strong>This case study assessed D-loop methylation levels in peripheral blood samples from 37 patients with PD, 18 patients with Parkinson's disease dementia (PD-D), 26 patients with atypical parkinsonism (APS), and 26 healthy controls (HC). Associations with clinical parameters, sex, and L-dopa treatment were analyzed.</p><p><strong>Results: </strong>D-loop methylation levels were significantly reduced in patients with PD-D and APS compared to PD patients and HC. Methylation levels were not associated with disease duration, clinical variables, sex, or L-dopa treatment.</p><p><strong>Conclusions: </strong>Decreased mitochondrial D-loop methylation in PD-D and APS may reflect disease-specific epigenetic mechanisms rather than clinical characteristics or treatment effects.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"197-204"},"PeriodicalIF":3.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156431","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":"Methylation changes of gallbladder DNA during the formation of gallstones.","authors":"Hongyu Xu, Jinlong Hu, Jinshan Liu, Rui Wang, Junbin Peng, Peilin Liu, Jiaming Yao, Baoqiang Cao","doi":"10.1080/17501911.2025.2610614","DOIUrl":"10.1080/17501911.2025.2610614","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the genome-wide methylation changes in gallbladder tissues during gallstone formation, as well as alterations in key signaling pathways and associated gene expression.</p><p><strong>Methods: </strong>A combined methylation and transcriptomic analysis was performed on gallbladder tissues from gallstone model mice and normal control mice using reduced representation bisulfite sequencing (RRBS) and RNA high-throughput sequencing. Key candidate genes were validated using qRT-PCR, Western blotting, and immunohistochemistry. Cross-species validation was conducted using human gallbladder transcriptomic data from GEO datasets.</p><p><strong>Results: </strong>Integrated RRBS and RNA-seq analysis revealed that abnormal DNA methylation may contribute to gallstone formation by dysregulating gene expression in pathways associated with gallbladder dysfunction. A total of 97 differentially methylated and expressed genes exhibiting significant inverse correlations between methylation and expression levels were identified. The top six genes with the strongest correlations were experimentally validated. Analysis of human gallstone samples identified partial overlapping differentially expressed genes with the mouse model.</p><p><strong>Conclusion: </strong>This study demonstrates the potential roles of DNA methylation and gene expression changes in gallbladder tissue during the formation of gallstones. These findings provide a new perspective for further understanding the causes of gallstones and searching for possible clinical therapies.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"55-71"},"PeriodicalIF":3.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145910793","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}
EpigenomicsPub Date : 2026-01-01Epub Date: 2025-12-23DOI: 10.1080/17501911.2025.2603883
Phyo W Win, Julia Nguyen, Elly H Shin, Tyler S Nagano, Brent Selimi, Katie Hong, Anahita M Meybodi, Bradley P Yates, Emma V Burke, David E Carter, Gregory A Newby, Charles Newcomb, Dan E Arking, Christina A Castellani
{"title":"Mitochondrial DNA copy number reduction via <i>in vitro TFAM</i> knockout remodels the nuclear epigenome and transcriptome.","authors":"Phyo W Win, Julia Nguyen, Elly H Shin, Tyler S Nagano, Brent Selimi, Katie Hong, Anahita M Meybodi, Bradley P Yates, Emma V Burke, David E Carter, Gregory A Newby, Charles Newcomb, Dan E Arking, Christina A Castellani","doi":"10.1080/17501911.2025.2603883","DOIUrl":"10.1080/17501911.2025.2603883","url":null,"abstract":"<p><strong>Aims: </strong>Mitochondrial DNA copy number (mtDNA-CN) is associated with several age-related chronic diseases and is a predictor of all-cause mortality. Here, we examine site-specific differential nuclear DNA (nDNA) methylation and differential gene expression resulting from in vitro reduction of mtDNA-CN to uncover shared genes and biological pathways mediating the effect of mtDNA-CN on disease.</p><p><strong>Materials and methods: </strong>Epigenome and transcriptome profiles were generated for three independent human embryonic kidney (HEK293T) cell lines harboring a mitochondrial transcription factor A (TFAM) knockout generated via CRISPR-Cas9, and matched control lines.</p><p><strong>Results: </strong>We identified 2924 differentially methylated sites, 67 differentially methylated regions, and 102 differentially expressed genes associated with mtDNA-CN. Integrated analysis uncovered 24 Gene-CpG pairs. GABA<sub>A</sub> receptor genes and related pathways, the neuroactive ligand signaling pathway, ABCD1/2 gene activity, and cell signaling processes were overrepresented, providing insight into the underlying biological mechanisms facilitating these associations. We also report evidence implicating chromatin state regulatory mechanisms as modulators of mtDNA-CN effect on gene expression.</p><p><strong>Conclusions: </strong>We demonstrate that mitochondrial DNA variation signals to the nuclear DNA epigenome and transcriptome and may lead to nuclear remodeling relevant to development, aging, and complex disease.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"27-44"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145810078","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}