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Pulmonary Pathogen-Induced Epigenetic Modifications. 肺部病原体诱导的表观遗传修饰。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-07-06 DOI: 10.3390/epigenomes7030013
Dylan Wrede, Mika Bordak, Yeabtsega Abraham, Masfique Mehedi

Epigenetics generally involves genetic control by factors other than our own DNA sequence. Recent research has focused on delineating the mechanisms of two major epigenetic phenomena: DNA methylation and histone modification. As epigenetics involves many cellular processes, it is no surprise that it can also influence disease-associated gene expression. A direct link between respiratory infections, host cell epigenetic regulations, and chronic lung diseases is still unknown. Recent studies have revealed bacterium- or virus-induced epigenetic changes in the host cells. In this review, we focused on respiratory pathogens (viruses, bacteria, and fungi) induced epigenetic modulations (DNA methylation and histone modification) that may contribute to lung disease pathophysiology by promoting host defense or allowing pathogen persistence.

表观遗传学通常是指基因受自身 DNA 序列以外的因素控制。近期研究的重点是阐明两大表观遗传现象的机制:DNA 甲基化和组蛋白修饰。由于表观遗传学涉及许多细胞过程,因此它也会影响疾病相关基因的表达,这并不奇怪。呼吸道感染、宿主细胞表观遗传调控和慢性肺部疾病之间的直接联系尚不清楚。最近的研究揭示了细菌或病毒诱导的宿主细胞表观遗传学变化。在这篇综述中,我们重点探讨了呼吸道病原体(病毒、细菌和真菌)诱导的表观遗传学调控(DNA 甲基化和组蛋白修饰),这些调控可能会促进宿主防御或允许病原体持续存在,从而对肺部疾病的病理生理学做出贡献。
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引用次数: 0
Therapeutic Applications of Azanucleoside Analogs as DNA Demethylating Agents. 氮杂核苷类似物作为DNA去甲基化剂的治疗应用。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-07-05 DOI: 10.3390/epigenomes7030012
Fallon Gallimore, Tamer E Fandy

Azanucleosides, such as 5-azacytidine and decitabine, are DNA demethylating agents used in the treatment of acute myeloid leukemia and myelodysplastic syndromes. Researchers continue to explore their utility in the treatment of other hematologic and solid tumors. Based on the capacity of the compounds to inhibit DNA methyltransferase enzymes and the important role of DNA methylation in health and disease, it is essential to understand the molecular changes that azanucleosides induce and how these changes may improve treatment outcomes in subsets of patients. This review summarizes the molecular and therapeutic actions of azanucleosides and discusses recent clinical trials of these compounds as single agents or in combination therapy for the treatment of cancer and related conditions.

氮杂核苷,如5-氮杂胞苷和地西他滨,是用于治疗急性髓性白血病和骨髓增生异常综合征的DNA去甲基化药物。研究人员继续探索其在其他血液学和实体肿瘤治疗中的应用。基于这些化合物抑制DNA甲基转移酶的能力以及DNA甲基化在健康和疾病中的重要作用,有必要了解氮杂核苷诱导的分子变化以及这些变化如何改善亚群患者的治疗结果。本文综述了氮杂核苷的分子和治疗作用,并讨论了这些化合物作为单一药物或联合治疗癌症及相关疾病的最新临床试验。
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引用次数: 0
Graft-Derived Cell-Free DNA Quantification following Liver Transplantation Using Tissue-Specific DNA Methylation and Donor-Specific Genotyping Techniques: An Orthogonal Comparison Study. 使用组织特异性DNA甲基化和供体特异性基因分型技术对肝移植后移植物来源的无细胞DNA进行定量:一项正交比较研究。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-06-09 DOI: 10.3390/epigenomes7020011
Daniel R A Cox, Tess McClure, Fan Zhang, Boris Ka Leong Wong, Adam Testro, Su Kah Goh, Vijayaragavan Muralidharan, Alexander Dobrovic

Background: Graft-derived cell-free DNA (gdcfDNA) analysis has shown promise as a non-invasive tool for monitoring organ health following solid organ transplantation. A number of gdcfDNA analysis techniques have been described; however, the majority rely on sequencing or prior genotyping to detect donor-recipient mis-matched genetic polymorphisms. Differentially methylated regions of DNA can be used to identify the tissue-of-origin of cell-free DNA (cfDNA) fragments. In this study, we aimed to directly compare the performance of gdcfDNA monitoring using graft-specific DNA methylation analysis and donor-recipient genotyping techniques in a pilot cohort of clinical samples from patients post-liver transplantation. Results: 7 patients were recruited prior to LT, 3 developed early, biopsy-proven TCMR in the first 6 weeks post-LT. gdcfDNA was successfully quantified in all samples using both approaches. There was a high level of technical correlation between results using the two techniques (Spearman testing, rs = 0.87, p < 0.0001). gdcfDNA levels quantified using the genotyping approach were significantly greater across all timepoints in comparison to the tissue-specific DNA methylation-based approach: e.g., day 1 post-LT median 31,350 copies/mL (IQR 6731-64,058) vs. 4133 copies/mL (IQR 1100-8422), respectively. Qualitative trends in gdcfDNA levels for each patient were concordant between the two assays. Acute TCMR was preceded by significant elevations in gdcfDNA as quantified by both techniques. Elevations in gdcfDNA, using both techniques, were suggestive of TCMR in this pilot study with a 6- and 3-day lead-time prior to histological diagnosis in patients 1 and 2. Conclusions: Both the graft-specific methylation and genotyping techniques successfully quantified gdcfDNA in patients post-LT with statistically significant concordance. A direct comparison of these two techniques is not only important from a technical perspective for orthogonal validation, but significantly adds weight to the evidence that gdcfDNA monitoring reflects the underlying biology. Both techniques identified LT recipients who developed acute TCMR, with several days lead-time in comparison to conventional diagnostic workflows. Whilst the two assays performed comparably, gdcfDNA monitoring based on graft-specific DNA methylation patterns in cfDNA offers major practical advantages over the donor-recipient genotyping, and hence enhances the potential to translate this emerging technology into clinical practice.

背景:移植物无细胞DNA (Graft-derived cell-free DNA, gdcfDNA)分析有望成为实体器官移植后监测器官健康的一种无创工具。一些gdcfDNA分析技术已经被描述;然而,大多数依赖于测序或先前的基因分型来检测供体-受体不匹配的遗传多态性。DNA的差异甲基化区域可用于鉴定无细胞DNA (cfDNA)片段的组织起源。在这项研究中,我们旨在直接比较使用移植物特异性DNA甲基化分析和供体-受体基因分型技术对肝移植后患者临床样本进行gdcfDNA监测的性能。结果:7名患者在肝移植前被招募,3名患者在肝移植后的前6周出现早期活检证实的TCMR。使用这两种方法,在所有样品中都成功地定量了gdcfDNA。使用这两种技术的结果之间存在高度的技术相关性(Spearman检验,rs = 0.87, p < 0.0001)。与基于组织特异性DNA甲基化的方法相比,使用基因分型方法量化的gdcfDNA水平在所有时间点上都显著更高:例如,lt后第1天的中位数分别为31,350拷贝/mL (IQR 6731-64,058)和4133拷贝/mL (IQR 1100-8422)。两种检测方法中每位患者gdcfDNA水平的定性趋势一致。在急性TCMR之前,两种技术都量化了gdcfDNA的显著升高。在本初步研究中,在患者1和2的组织学诊断前6天和3天,使用这两种技术的gdcfDNA升高提示TCMR。结论:移植物特异性甲基化和基因分型技术都成功地量化了移植后患者的gdcfDNA,具有统计学意义的一致性。这两种技术的直接比较不仅从正交验证的技术角度来说很重要,而且显著地增加了gdcfDNA监测反映潜在生物学的证据的权重。与传统的诊断工作流程相比,这两种技术都可以在几天的时间内确定出现急性TCMR的肝移植受体。虽然这两种检测方法的效果相当,但基于移植物特异性DNA甲基化模式的gdcfDNA监测比供体-受体基因分型具有主要的实用优势,因此增强了将这一新兴技术转化为临床实践的潜力。
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引用次数: 0
Histone Demethylase Modulation: Epigenetic Strategy to Combat Cancer Progression. 组蛋白去甲基化酶调节:对抗癌症进展的表观遗传策略。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-05-17 DOI: 10.3390/epigenomes7020010
Rashmi Srivastava, Rubi Singh, Shaurya Jauhari, Niraj Lodhi, Rakesh Srivastava
Epigenetic modifications are heritable, reversible changes in histones or the DNA that control gene functions, being exogenous to the genomic sequence itself. Human diseases, particularly cancer, are frequently connected to epigenetic dysregulations. One of them is histone methylation, which is a dynamically reversible and synchronously regulated process that orchestrates the three-dimensional epigenome, nuclear processes of transcription, DNA repair, cell cycle, and epigenetic functions, by adding or removing methylation groups to histones. Over the past few years, reversible histone methylation has become recognized as a crucial regulatory mechanism for the epigenome. With the development of numerous medications that target epigenetic regulators, epigenome-targeted therapy has been used in the treatment of malignancies and has shown meaningful therapeutic potential in preclinical and clinical trials. The present review focuses on the recent advances in our knowledge on the role of histone demethylases in tumor development and modulation, in emphasizing molecular mechanisms that control cancer cell progression. Finally, we emphasize current developments in the advent of new molecular inhibitors that target histone demethylases to regulate cancer progression.
表观遗传修饰是控制基因功能的组蛋白或DNA的可遗传的、可逆的变化,对基因组序列本身是外源的。人类疾病,特别是癌症,经常与表观遗传失调有关。其中之一是组蛋白甲基化,这是一个动态可逆和同步调节的过程,通过在组蛋白上添加或删除甲基化基团,协调三维表观基因组,转录,DNA修复,细胞周期和表观遗传功能的核过程。在过去的几年中,可逆性组蛋白甲基化已被认为是表观基因组的重要调控机制。随着许多靶向表观遗传调控因子的药物的发展,表观基因组靶向治疗已被用于恶性肿瘤的治疗,并在临床前和临床试验中显示出有意义的治疗潜力。本文综述了组蛋白去甲基化酶在肿瘤发生和调节中的作用的最新进展,强调了控制癌细胞进展的分子机制。最后,我们强调了目前新分子抑制剂的发展,这些抑制剂靶向组蛋白去甲基化酶来调节癌症的进展。
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引用次数: 0
Critical Considerations for Investigating MicroRNAs during Tumorigenesis: A Case Study in Conceptual and Contextual Nuances of miR-211-5p in Melanoma. 研究肿瘤发生过程中 MicroRNA 的关键因素:黑色素瘤中 miR-211-5p 的概念和内涵细微差别案例研究》。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-04-26 DOI: 10.3390/epigenomes7020009
Fatemeh Vand-Rajabpour, Meghan Savage, Rachel L Belote, Robert L Judson-Torres

MicroRNAs are non-coding RNAs fundamental to metazoan development and disease. Although the aberrant regulation of microRNAs during mammalian tumorigenesis is well established, investigations into the contributions of individual microRNAs are wrought with conflicting observations. The underlying cause of these inconsistencies is often attributed to context-specific functions of microRNAs. We propose that consideration of both context-specific factors, as well as underappreciated fundamental concepts of microRNA biology, will permit a more harmonious interpretation of ostensibly diverging data. We discuss the theory that the biological function of microRNAs is to confer robustness to specific cell states. Through this lens, we then consider the role of miR-211-5p in melanoma progression. Using literature review and meta-analyses, we demonstrate how a deep understating of domain-specific contexts is critical for moving toward a concordant understanding of miR-211-5p and other microRNAs in cancer biology.

微小RNA是一种非编码RNA,对后生动物的发育和疾病至关重要。尽管在哺乳动物肿瘤发生过程中,microRNAs 的异常调控已得到公认,但对单个 microRNAs 的贡献的研究结果却相互矛盾。这些不一致的根本原因通常归咎于 microRNA 的特定环境功能。我们建议,同时考虑特定环境因素和未被充分重视的 microRNA 生物学基本概念,可以更和谐地解释表面上存在分歧的数据。我们讨论了 microRNA 的生物学功能是赋予特定细胞状态稳健性的理论。通过这一视角,我们将探讨 miR-211-5p 在黑色素瘤进展中的作用。通过文献综述和荟萃分析,我们证明了深入了解特定领域的背景对于统一认识 miR-211-5p 和其他 microRNA 在癌症生物学中的作用至关重要。
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引用次数: 0
Epigenome-Wide Changes in the Cell Layers of the Vein Wall When Exposing the Venous Endothelium to Oscillatory Shear Stress. 当静脉内皮暴露于振荡剪切应力时,静脉壁细胞层的全表观基因组变化。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-03-20 DOI: 10.3390/epigenomes7010008
Mariya A Smetanina, Valeria A Korolenya, Alexander E Kel, Ksenia S Sevostyanova, Konstantin A Gavrilov, Andrey I Shevela, Maxim L Filipenko

Epigenomic changes in the venous cells exerted by oscillatory shear stress towards the endothelium may result in consolidation of gene expression alterations upon vein wall remodeling during varicose transformation. We aimed to reveal such epigenome-wide methylation changes. Primary culture cells were obtained from non-varicose vein segments left after surgery of 3 patients by growing the cells in selective media after magnetic immunosorting. Endothelial cells were either exposed to oscillatory shear stress or left at the static condition. Then, other cell types were treated with preconditioned media from the adjacent layer's cells. DNA isolated from the harvested cells was subjected to epigenome-wide study using Illumina microarrays followed by data analysis with GenomeStudio (Illumina), Excel (Microsoft), and Genome Enhancer (geneXplain) software packages. Differential (hypo-/hyper-) methylation was revealed for each cell layer's DNA. The most targetable master regulators controlling the activity of certain transcription factors regulating the genes near the differentially methylated sites appeared to be the following: (1) HGS, PDGFB, and AR for endothelial cells; (2) HGS, CDH2, SPRY2, SMAD2, ZFYVE9, and P2RY1 for smooth muscle cells; and (3) WWOX, F8, IGF2R, NFKB1, RELA, SOCS1, and FXN for fibroblasts. Some of the identified master regulators may serve as promising druggable targets for treating varicose veins in the future.

在静脉曲张转化过程中,振荡剪应力对内皮施加的静脉细胞的表观基因组变化可能导致静脉壁重塑过程中基因表达改变的巩固。我们的目的是揭示这种表观基因组范围内的甲基化变化。从3例患者术后留下的非曲张静脉段中提取细胞,经磁免疫分选,在选择性培养基中培养,获得原代培养细胞。内皮细胞被暴露在振荡剪切应力下或处于静止状态。然后,用邻近层细胞的预处理培养基处理其他细胞类型。从收获的细胞中分离的DNA使用Illumina微阵列进行全表观基因组研究,然后使用GenomeStudio (Illumina)、Excel (Microsoft)和Genome Enhancer (geneXplain)软件包进行数据分析。不同细胞层的DNA甲基化程度不同(低/高)。控制某些转录因子活性的最可靶向的主调节剂似乎是以下几种:(1)内皮细胞的HGS、PDGFB和AR;(2)平滑肌细胞的HGS、CDH2、SPRY2、SMAD2、ZFYVE9、P2RY1;(3)成纤维细胞的WWOX、F8、IGF2R、NFKB1、RELA、SOCS1和FXN。一些已确定的主调控因子可能成为未来治疗静脉曲张的有希望的药物靶点。
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引用次数: 0
Chemical Inhibitors Targeting the Histone Lysine Demethylase Families with Potential for Drug Discovery. 靶向组蛋白赖氨酸去甲基酶家族的化学抑制剂与潜在的药物发现。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-03-11 DOI: 10.3390/epigenomes7010007
Nando Dulal Das, Hideaki Niwa, Takashi Umehara

The dynamic regulation of histone methylation and demethylation plays an important role in the regulation of gene expression. Aberrant expression of histone lysine demethylases has been implicated in various diseases including intractable cancers, and thus lysine demethylases serve as promising therapeutic targets. Recent studies in epigenomics and chemical biology have led to the development of a series of small-molecule demethylase inhibitors that are potent, specific, and have in vivo efficacy. In this review, we highlight emerging small-molecule inhibitors targeting the histone lysine demethylases and their progress toward drug discovery.

组蛋白甲基化和去甲基化的动态调控在基因表达调控中起着重要作用。组蛋白赖氨酸去甲基化酶的异常表达与包括难治性癌症在内的多种疾病有关,因此赖氨酸去甲基化酶是有希望的治疗靶点。近年来,表观基因组学和化学生物学的研究导致了一系列小分子去甲基酶抑制剂的发展,这些抑制剂是有效的,特异性的,并且在体内有效。在这篇综述中,我们重点介绍了针对组蛋白赖氨酸去甲基化酶的新出现的小分子抑制剂及其在药物发现方面的进展。
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引用次数: 1
Epigenetic Regulation in Breast Cancer: Insights on Epidrugs. 乳腺癌的表观遗传调控:外源性药物的见解。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-02-18 DOI: 10.3390/epigenomes7010006
Ayoung Kim, Kyumin Mo, Hyeonseok Kwon, Soohyun Choe, Misung Park, Woori Kwak, Hyunho Yoon

Breast cancer remains a common cause of cancer-related death in women. Therefore, further studies are necessary for the comprehension of breast cancer and the revolution of breast cancer treatment. Cancer is a heterogeneous disease that results from epigenetic alterations in normal cells. Aberrant epigenetic regulation is strongly associated with the development of breast cancer. Current therapeutic approaches target epigenetic alterations rather than genetic mutations due to their reversibility. The formation and maintenance of epigenetic changes depend on specific enzymes, including DNA methyltransferases and histone deacetylases, which are promising targets for epigenetic-based therapy. Epidrugs target different epigenetic alterations, including DNA methylation, histone acetylation, and histone methylation, which can restore normal cellular memory in cancerous diseases. Epigenetic-targeted therapy using epidrugs has anti-tumor effects on malignancies, including breast cancer. This review focuses on the importance of epigenetic regulation and the clinical implications of epidrugs in breast cancer.

乳腺癌仍然是妇女癌症相关死亡的常见原因。因此,进一步的研究对于了解乳腺癌和乳腺癌治疗的革命是必要的。癌症是一种异质性疾病,由正常细胞的表观遗传改变引起。异常的表观遗传调控与乳腺癌的发生密切相关。由于其可逆性,目前的治疗方法针对表观遗传改变而不是基因突变。表观遗传变化的形成和维持依赖于特定的酶,包括DNA甲基转移酶和组蛋白去乙酰化酶,它们是基于表观遗传治疗的有希望的靶点。外源性药物针对不同的表观遗传改变,包括DNA甲基化、组蛋白乙酰化和组蛋白甲基化,这些改变可以恢复癌变疾病的正常细胞记忆。使用外用药物的表观遗传靶向治疗对包括乳腺癌在内的恶性肿瘤具有抗肿瘤作用。本文综述了表观遗传调控在乳腺癌中的重要性以及外源性药物的临床意义。
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引用次数: 5
SNCA Gene Methylation in Parkinson's Disease and Multiple System Atrophy. SNCA基因甲基化在帕金森病和多系统萎缩中的作用
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-02-06 DOI: 10.3390/epigenomes7010005
Ekaterina Yu Fedotova, Elena V Iakovenko, Natalia Yu Abramycheva, Sergey N Illarioshkin

In recent years, epigenetic mechanisms have been implicated in the development of multifactorial diseases including neurodegenerative disorders. In Parkinson's disease (PD), as a synucleinopathy, most studies focused on DNA methylation of SNCA gene coding alpha-synuclein but obtained results were rather contradictory. In another neurodegenerative synucleinopathy, multiple system atrophy (MSA), very few studies investigated the epigenetic regulation. This study included patients with PD (n = 82), patients with MSA (n = 24), and a control group (n = 50). In three groups, methylation levels of CpG and non-CpG sites in regulatory regions of the SNCA gene were analyzed. We revealed hypomethylation of CpG sites in the SNCA intron 1 in PD and hypermethylation of predominantly non-CpG sites in the SNCA promoter region in MSA. In PD patients, hypomethylation in the intron 1 was associated with earlier age at the disease onset. In MSA patients, hypermethylation in the promotor was associated with shorter disease duration (before examination). These results showed different patterns of the epigenetic regulation in two synucleinopathies-PD and MSA.

近年来,表观遗传机制已涉及多因素疾病的发展,包括神经退行性疾病。在帕金森病(PD)中,作为一种突触核蛋白病,大多数研究都集中在编码α -突触核蛋白的SNCA基因的DNA甲基化上,但得到的结果却相当矛盾。在另一种神经退行性突触核蛋白病,多系统萎缩(MSA)中,很少有研究研究表观遗传调控。本研究包括PD患者(n = 82)、MSA患者(n = 24)和对照组(n = 50)。在三组中,分析SNCA基因调控区域CpG和非CpG位点的甲基化水平。我们发现PD中SNCA内含子1中CpG位点的低甲基化和MSA中SNCA启动子区域主要非CpG位点的高甲基化。在PD患者中,内含子1的低甲基化与疾病发病年龄较早有关。在MSA患者中,启动子的高甲基化与较短的疾病持续时间(检查前)相关。这些结果表明pd和MSA两种突触核蛋白病的表观遗传调控模式不同。
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引用次数: 1
DNA Methylation Is a Potential Biomarker for Cardiometabolic Health in Mexican Children and Adolescents. DNA 甲基化是墨西哥儿童和青少年心脏代谢健康的潜在生物标志物。
IF 2.5 Q3 GENETICS & HEREDITY Pub Date : 2023-02-03 DOI: 10.3390/epigenomes7010004
Abeer A Aljahdali, Jaclyn M Goodrich, Dana C Dolinoy, Hyungjin M Kim, Edward A Ruiz-Narváez, Ana Baylin, Alejandra Cantoral, Libni A Torres-Olascoaga, Martha M Téllez-Rojo, Karen E Peterson

DNA methylation (DNAm) is a plausible mechanism underlying cardiometabolic abnormalities, but evidence is limited among youth. This analysis included 410 offspring of the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) birth cohort followed up to two time points in late childhood/adolescence. At Time 1, DNAm was quantified in blood leukocytes at long interspersed nuclear elements (LINE-1), H19, and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), and at Time 2 in peroxisome proliferator-activated receptor alpha (PPAR-α). At each time point, cardiometabolic risk factors were assessed including lipid profiles, glucose, blood pressure, and anthropometry. Linear mixed effects models were used for LINE-1, H19, and 11β-HSD-2 to account for the repeated-measure outcomes. Linear regression models were conducted for the cross-sectional association between PPAR-α with the outcomes. DNAm at LINE-1 was associated with log glucose at site 1 [β = -0.029, p = 0.0006] and with log high-density lipoprotein cholesterol at site 3 [β = 0.063, p = 0.0072]. 11β-HSD-2 DNAm at site 4 was associated with log glucose (β = -0.018, p = 0.0018). DNAm at LINE-1 and 11β-HSD-2 was associated with few cardiometabolic risk factors among youth in a locus-specific manner. These findings underscore the potential for epigenetic biomarkers to increase our understanding of cardiometabolic risk earlier in life.

DNA甲基化(DNAm)是心血管代谢异常的一种合理机制,但在青少年中证据有限。这项分析包括对墨西哥早期生活暴露于环境有毒物质(ELEMENT)出生队列中的 410 名后代进行跟踪调查,直至儿童晚期/青春期的两个时间点。在第 1 个时间点,对血液白细胞中长间隔核元素(LINE-1)、H19 和 11β- 羟类固醇脱氢酶 2 型(11β-HSD-2)的 DNAm 进行量化;在第 2 个时间点,对过氧化物酶体增殖激活受体α(PPAR-α)的 DNAm 进行量化。在每个时间点,都对心脏代谢风险因素进行了评估,包括血脂、血糖、血压和人体测量。对LINE-1、H19和11β-HSD-2采用线性混合效应模型,以考虑重复测量结果。对 PPAR-α 与结果之间的横截面关系进行了线性回归模型分析。LINE-1 上的 DNAm 与第 1 位点的葡萄糖对数相关[β = -0.029,p = 0.0006],与第 3 位点的高密度脂蛋白胆固醇对数相关[β = 0.063,p = 0.0072]。位点 4 上的 11β-HSD-2 DNAm 与葡萄糖对数相关(β = -0.018,p = 0.0018)。LINE-1和11β-HSD-2基因位点的DNAm以位点特异性的方式与青少年的一些心脏代谢风险因素相关。这些发现强调了表观遗传生物标志物的潜力,有助于我们加深对生命早期心脏代谢风险的了解。
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引用次数: 0
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