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本文引用的文献

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Correction: "Congenital hyperinsulinism as the presenting feature of Kabuki syndrome: clinical and molecular characterization of 10 affected individuals".更正:“先天性高胰岛素血症作为歌舞伎综合征的首发特征:10例受累个体的临床和分子特征”
Genet Med. 2019 Jan;21(1):262-265. doi: 10.1038/s41436-018-0126-1.
2
Epigenome-wide association study of adiposity and future risk of obesity-related diseases.肥胖症与肥胖相关疾病未来发病风险的表观基因组关联研究。
Int J Obes (Lond). 2018 Dec;42(12):2022-2035. doi: 10.1038/s41366-018-0064-7. Epub 2018 May 1.
3
The NIEHS TaRGET II Consortium and environmental epigenomics.美国国立环境卫生科学研究所第二代风险基因与环境表观基因组学研究联盟
Nat Biotechnol. 2018 Mar 6;36(3):225-227. doi: 10.1038/nbt.4099.
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The Landscape of Histone Modifications in a High-Fat Diet-Induced Obese (DIO) Mouse Model.高脂饮食诱导肥胖(DIO)小鼠模型中的组蛋白修饰图谱
Mol Cell Proteomics. 2017 Jul;16(7):1324-1334. doi: 10.1074/mcp.M117.067553. Epub 2017 Apr 27.
5
A novel identified circular RNA, circRNA_010567, promotes myocardial fibrosis via suppressing miR-141 by targeting TGF-β1.一种新鉴定出的环状RNA,即circRNA_010567,通过靶向转化生长因子-β1(TGF-β1)抑制miR-141来促进心肌纤维化。
Biochem Biophys Res Commun. 2017 Jun 10;487(4):769-775. doi: 10.1016/j.bbrc.2017.04.044. Epub 2017 Apr 12.
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Genome-wide hepatic DNA methylation changes in high-fat diet-induced obese mice.高脂饮食诱导的肥胖小鼠肝脏全基因组DNA甲基化变化
Nutr Res Pract. 2017 Apr;11(2):105-113. doi: 10.4162/nrp.2017.11.2.105. Epub 2017 Mar 15.
7
The histone H3K9 methyltransferase SUV39H links SIRT1 repression to myocardial infarction.组蛋白 H3K9 甲基转移酶 SUV39H 将 SIRT1 抑制与心肌梗死联系起来。
Nat Commun. 2017 Mar 31;8:14941. doi: 10.1038/ncomms14941.
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A MicroRNA93-Interferon Regulatory Factor-9-Immunoresponsive Gene-1-Itaconic Acid Pathway Modulates M2-Like Macrophage Polarization to Revascularize Ischemic Muscle.一种微小RNA93-干扰素调节因子9-免疫反应基因1-衣康酸途径调节M2样巨噬细胞极化以促进缺血肌肉血管再生。
Circulation. 2017 Jun 13;135(24):2403-2425. doi: 10.1161/CIRCULATIONAHA.116.025490. Epub 2017 Mar 29.
9
Metabolic Syndrome Prevalence by Race/Ethnicity and Sex in the United States, National Health and Nutrition Examination Survey, 1988-2012.1988 - 2012年美国国家健康与营养检查调查中按种族/族裔和性别划分的代谢综合征患病率
Prev Chronic Dis. 2017 Mar 16;14:E24. doi: 10.5888/pcd14.160287.
10
miR-146a mediates inflammatory changes and fibrosis in the heart in diabetes.微小RNA-146a介导糖尿病患者心脏的炎症变化和纤维化。
J Mol Cell Cardiol. 2017 Apr;105:70-76. doi: 10.1016/j.yjmcc.2017.03.002. Epub 2017 Mar 6.

代谢综合征的表观遗传学。

Epigenetics of metabolic syndrome.

机构信息

Department of Genetics, Washington University School of Medicine , Saint Louis, Missouri.

出版信息

Physiol Genomics. 2018 Nov 1;50(11):947-955. doi: 10.1152/physiolgenomics.00072.2018. Epub 2018 Sep 21.

DOI:10.1152/physiolgenomics.00072.2018
PMID:30240346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6293117/
Abstract

The dramatic increase in global prevalence of metabolic disease is inexplicable when considering only environmental or only genetic factors, leading to the need to explore the possible roles of epigenetic factors. A great deal of progress has been made in this interdisciplinary field in recent years, with many studies investigating various aspects of the metabolic syndrome and its associated epigenetic changes. Rodent models of metabolic diseases have been particularly illuminating because of the ability to leverage tools such as genetic and environmental modifications. The current review summarizes recent breakthroughs regarding epigenetic markers in studies of obesity, Type II diabetes, and cardiovascular disease, the three major disorders associated with metabolic syndrome. We also discuss open questions and future directions for integrating genomic, epigenomic, and phenotypic big biodata toward understanding metabolic syndrome etiology.

摘要

当仅考虑环境或遗传因素时,全球代谢性疾病患病率的急剧上升是无法解释的,这促使人们需要探索表观遗传因素的可能作用。近年来,这个跨学科领域取得了很大的进展,许多研究调查了代谢综合征及其相关表观遗传变化的各个方面。代谢性疾病的啮齿动物模型特别有启发性,因为能够利用遗传和环境修饰等工具。本综述总结了肥胖症、2 型糖尿病和心血管疾病(与代谢综合征相关的三大疾病)研究中有关表观遗传标记物的最新突破。我们还讨论了整合基因组、表观基因组和表型大生物数据以了解代谢综合征病因的一些开放性问题和未来方向。