Epigenetics in Cardiac Hypertrophy and Heart Failure

被引:88
作者
Liu, Chia-Feng [1 ]
Tang, W. H. Wilson [1 ,2 ]
机构
[1] Cleveland Clin, Dept Cardiovasc & Metab Sci, Lerner Res Inst, Cleveland, OH 44195 USA
[2] Cleveland Clin, Heart & Vasc Inst, Dept Cardiovasc Med, 950o Euclid Ave,Desk J3-4, Cleveland, OH 44195 USA
基金
美国国家卫生研究院;
关键词
cardiac hypertrophy; epigenetics; heart failure;
D O I
10.1016/j.jacbts.2019.05.011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Heart failure (HF) is a complex syndrome affecting millions of people around the world. Over the past decade, the therapeutic potential of targeting epigenetic regulators in HF has been discussed extensively. Recent advances in next-generation sequencing techniques have contributed substantial progress in our understanding of the role of DNA methylation, post-translational modifications of histones, adenosine triphosphate (ATP)-dependent chromatin conformation and remodeling, and non-coding RNAs in HF pathophysiology. In this review, we summarize epigenomic studies on human and animal. models in HF. (C) 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.
引用
收藏
页码:976 / 993
页数:18
相关论文
共 117 条
[1]   The histone variant H3.3 marks active chromatin by replication-independent nucleosome assembly [J].
Ahmad, K ;
Henikoff, S .
MOLECULAR CELL, 2002, 9 (06) :1191-1200
[2]   Diet, Gut Microbiome and Epigenetics: Emerging Links with Inflammatory Bowel Diseases and Prospects for Management and Prevention [J].
Aleksandrova, Krasimira ;
Romero-Mosquera, Beatriz ;
Hernandez, Vicent .
NUTRIENTS, 2017, 9 (09) :1-13
[3]   A Novel Highly Bioavailable Curcumin Formulation Improves Symptoms and Diagnostic Indicators in Rheumatoid Arthritis Patients: A Randomized, Double-Blind, Placebo-Controlled, Two-Dose, Three-Arm, and Parallel-Group Study [J].
Amalraj, Augustine ;
Varma, Karthik ;
Jacob, Joby ;
Divya, Chandradhara ;
Kunnumakkara, Ajaikumar B. ;
Stohs, Sidney J. ;
Gopi, Sreeraj .
JOURNAL OF MEDICINAL FOOD, 2017, 20 (10) :1022-1030
[4]   BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [J].
Anand, Priti ;
Brown, Jonathan D. ;
Lin, Charles Y. ;
Qi, Jun ;
Zhang, Rongli ;
Artero, Pedro Calderon ;
Alaiti, M. Amer ;
Bullard, Jace ;
Alazem, Kareem ;
Margulies, Kenneth B. ;
Cappola, Thomas P. ;
Lemieux, Madeleine ;
Plutzky, Jorge ;
Bradner, James E. ;
Haldar, Saptarsi M. .
CELL, 2013, 154 (03) :569-582
[5]  
Andoh A, 1999, CLIN EXP IMMUNOL, V118, P23
[6]   DOT1L, the H3K79 methyltransferase, is required for MLL-AF9-mediated leukemogenesis [J].
Anh Tram Nguyen ;
Taranova, Olena ;
He, Jin ;
Zhang, Yi .
BLOOD, 2011, 117 (25) :6912-6922
[7]   Butyrate and propionate induced activated or non-activated neutrophil apoptosis via HDAC inhibitor activity but without activating GPR-41/GPR-43 pathways [J].
Aoyama, Michiko ;
Kotani, Joji ;
Usami, Makoto .
NUTRITION, 2010, 26 (06) :653-661
[8]   Non-targeted metabolomics of Brg1/Brm double-mutant cardiomyocytes reveals a novel role for SWI/SNF complexes in metabolic homeostasis [J].
Banerjee, Ranjan ;
Bultman, Scott J. ;
Holley, Darcy ;
Hillhouse, Carolyn ;
Bain, James R. ;
Newgard, Christopher B. ;
Muehlbauer, Michael J. ;
Willis, Monte S. .
METABOLOMICS, 2015, 11 (05) :1287-1301
[9]   Circular noncoding RNAs as potential therapies and circulating biomarkers for cardiovascular diseases [J].
Bayoumi, Ahmed S. ;
Aonuma, Tatsuya ;
Teoh, Jian-peng ;
Tang, Yao-liang ;
Kim, Il-man .
ACTA PHARMACOLOGICA SINICA, 2018, 39 (07) :1100-1109
[10]   SWI/SNF chromatin-remodeling complexes in cardiovascular development and disease [J].
Bevilacqua, Ariana ;
Willis, Monte S. ;
Bultman, Scott J. .
CARDIOVASCULAR PATHOLOGY, 2014, 23 (02) :85-91