Epigenetics of metabolic syndrome

被引:34
|
作者
Carson, Caryn [1 ]
Lawson, Heather A. [1 ]
机构
[1] Washington Univ, Sch Med, Dept Genet, 660 S Euclid Ave,Campus Box 8232, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
cardiovascular disease; chromatin; epigenetics; histone modifications; metabolic syndrome; methylation; non-coding RNA; obesity; Type II diabetes; EPIGENOME-WIDE ASSOCIATION; DNA METHYLATION; GENE-EXPRESSION; ADIPOSE-TISSUE; MACROPHAGE POLARIZATION; DEVELOPMENTAL ORIGINS; GLUCOSE-HOMEOSTASIS; INSULIN-RESISTANCE; NONCODING RNA; UNITED-STATES;
D O I
10.1152/physiolgenomics.00072.2018
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:947 / 955
页数:9
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