Oxidative stress and DNA methylation regulation in the metabolic syndrome

被引:4
作者
Yara, Sabrina [1 ]
lavoie, Jean-ClauDe [1 ,2 ]
Levy, Emile [1 ,2 ]
机构
[1] Univ Montreal, CHU St Justine, Res Ctr, Fac Med, Montreal, PQ H3T 1C5, Canada
[2] Univ Montreal, Dept Nutr, Montreal, PQ H3T 1C5, Canada
关键词
antioxidant defense; DNA methylation; fetal programming; inflammation; metabolic syndrome; nutrition; oxidative stress; EXTRACELLULAR-SUPEROXIDE DISMUTASE; INTRAUTERINE GROWTH-RETARDATION; DIETARY-PROTEIN RESTRICTION; FOLIC-ACID SUPPLEMENTATION; RENIN-ANGIOTENSIN SYSTEM; DE-NOVO METHYLATION; FREE-RADICAL THEORY; EPIGENETIC REGULATION; INSULIN-RESISTANCE; NADPH OXIDASE;
D O I
10.2217/EPI.14.84
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
DNA methylation is implicated in tissue-specific gene expression and genomic imprinting. It is modulated by environmental factors, especially nutrition. Modified DNA methylation patterns may contribute to health problems and susceptibility to complex diseases. Current advances have suggested that the metabolic syndrome (MS) is a programmable disease, which is characterized by epigenetic modifications of vital genes when exposed to oxidative stress. Therefore, the main objective of this paper is to critically review the central context of MS while presenting the most recent knowledge related to epigenetic alterations that are promoted by oxidative stress. Potential pro-oxidant mechanisms that orchestrate changes in methylation profiling and are related to obesity, diabetes and hypertension are discussed. It is anticipated that the identification and understanding of the role of DNA methylation marks could be used to uncover early predictors and define drugs or diet-related treatments able to delay or reverse epigenetic changes, thereby combating MS burden.
引用
收藏
页码:283 / 300
页数:18
相关论文
共 151 条
[1]   New Nucleophilic Mechanisms of Ros-Dependent Epigenetic Modifications: Comparison of Aging and Cancer [J].
Afanas'ev, Igor .
AGING AND DISEASE, 2014, 5 (01) :52-62
[2]   Epigenetic Attenuation of Mitochondrial Superoxide Dismutase 2 in Pulmonary Arterial Hypertension A Basis for Excessive Cell Proliferation and a New Therapeutic Target [J].
Archer, Stephen L. ;
Marsboom, Glenn ;
Kim, Gene H. ;
Zhang, Hannah J. ;
Toth, Peter T. ;
Svensson, Eric C. ;
Dyck, Jason R. B. ;
Gomberg-Maitland, Mardi ;
Thebaud, Bernard ;
Husain, Aliya N. ;
Cipriani, Nicole ;
Rehman, Jalees .
CIRCULATION, 2010, 121 (24) :2661-U108
[3]  
Arnaud Philippe, 2005, Birth Defects Res C Embryo Today, V75, P81, DOI 10.1002/bdrc.20039
[4]   Non-CpG Methylation of the PGC-1α Promoter through DNMT3B Controls Mitochondrial Density [J].
Barres, Romain ;
Osler, Megan E. ;
Yan, Jie ;
Rune, Anna ;
Fritz, Tomas ;
Caidahl, Kenneth ;
Krook, Anna ;
Zierath, Juleen R. .
CELL METABOLISM, 2009, 10 (03) :189-198
[5]   Epigenetics: Connecting Environment and Genotype to Phenotype and Disease [J].
Barros, S. P. ;
Offenbacher, S. .
JOURNAL OF DENTAL RESEARCH, 2009, 88 (05) :400-408
[6]   LOSS OF METHYLATION ACTIVATES XIST IN SOMATIC BUT NOT IN EMBRYONIC-CELLS [J].
BEARD, C ;
LI, E ;
JAENISCH, R .
GENES & DEVELOPMENT, 1995, 9 (19) :2325-2334
[7]   The free radical theory of aging matures [J].
Beckman, KB ;
Ames, BN .
PHYSIOLOGICAL REVIEWS, 1998, 78 (02) :547-581
[8]   Oxidative stress and vascular damage in hypertension [J].
Berry, C ;
Brosnan, MJ ;
Fennell, J ;
Hamilton, CA ;
Dominiczak, AF .
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 2001, 10 (02) :247-255
[9]   CPG ISLANDS IN MAMMALIAN GENE PROMOTERS ARE INHERENTLY RESISTANT TO DENOVO METHYLATION [J].
BESTOR, TH ;
GUNDERSEN, G ;
KOLSTO, AB ;
PRYDZ, H .
GENETIC ANALYSIS-BIOMOLECULAR ENGINEERING, 1992, 9 (02) :48-53
[10]   The DNA methyltransferases of mammals [J].
Bestor, TH .
HUMAN MOLECULAR GENETICS, 2000, 9 (16) :2395-2402