Chromatin Remodeling in Cardiovascular Development and Physiology

被引：118
作者：
Han, Pei [1 ]
Hang, Calvin T. [1 ]
Yang, Jin [1 ]
Chang, Ching-Pin [1 ]
机构：
[1] Stanford Univ, Sch Med, Dept Med, Stanford Cardiovasc Inst,Div Cardiovasc Med, Stanford, CA 94305 USA
来源：
CIRCULATION RESEARCH | 2011年 / 108卷 / 03期
关键词：
chromatin; epigenetics; heart development; cardiomyopathy; gene expression; MYOSIN HEAVY-CHAIN; II HISTONE DEACETYLASES; MEF2 TRANSCRIPTION FACTOR; APOPTOSIS-INDUCING FACTOR; WOLF-HIRSCHHORN-SYNDROME; POLY(ADP-RIBOSE) POLYMERASE INHIBITION; GLYCOGEN-SYNTHASE KINASE-3-BETA; CARDIAC MYOCYTE PROLIFERATION; HEART-FAILURE; GENE-EXPRESSION;
D O I：
10.1161/CIRCRESAHA.110.224287
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Chromatin regulation provides an important means for controlling cardiac gene expression under different physiological and pathological conditions. Processes that direct the development of normal embryonic hearts and pathology of stressed adult hearts may share general mechanisms that govern cardiac gene expression by chromatin-regulating factors. These common mechanisms may provide a framework for us to investigate the interactions among diverse chromatin remodelers/modifiers and various transcription factors in the fine regulation of gene expression, essential for all aspects of cardiovascular biology. Aberrant cardiac gene expression, triggered by a variety of pathological insults, can cause heart diseases in both animals and humans. The severity of cardiomyopathy and heart failure correlates strongly with abnormal cardiac gene expression. Therefore, controlling cardiac gene expression presents a promising approach to the treatment of human cardiomyopathy. This review focuses on the roles of ATP-dependent chromatin-remodeling factors and chromatin-modifying enzymes in the control of gene expression during cardiovascular development and disease. (Circ Res. 2011;108:378-396.)
引用
收藏
页码：378 / 396
页数：19
相关论文
共 185 条
[1]   Coordinate changes in myosin heavy chain isoform gene expression are selectively associated with alterations in dilated cardiomyopathy phenotype [J].
Abraham, WT ;
Gilbert, EM ;
Lowes, BD ;
Minobe, WA ;
Larrabee, P ;
Roden, RL ;
Dutcher, D ;
Sederberg, J ;
Lindenfeld, JA ;
Wolfel, EE ;
Shakar, SF ;
Ferguson, D ;
Volkman, K ;
Linseman, JV ;
Quaife, RA ;
Robertson, AD ;
Bristow, MR .
MOLECULAR MEDICINE, 2002, 8 (11) :750-760
[2]   Sirt1 regulates aging and resistance to oxidative stress in the heart [J].
Alcendor, Ralph R. ;
Gao, Shumin ;
Zhai, Peiyong ;
Zablocki, Daniela ;
Holle, Eric ;
Yu, Xianzhong ;
Tian, Bin ;
Wagner, Thomas ;
Vatner, Stephen F. ;
Sadoshima, Junichi .
CIRCULATION RESEARCH, 2007, 100 (10) :1512-1521
[3]   Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo [J].
Antos, CL ;
McKinsey, TA ;
Frey, N ;
Kutschke, W ;
McAnally, J ;
Shelton, JM ;
Richardson, JA ;
Hill, JA ;
Olson, EN .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (02) :907-912
[4]   Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors [J].
Antos, CL ;
McKinsey, TA ;
Dreitz, M ;
Hollingsworth, LM ;
Zhang, CL ;
Schreiber, K ;
Rindt, H ;
Gorczynski, RJ ;
Olson, EN .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (31) :28930-28937
[5]   Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration [J].
Araki, T ;
Sasaki, Y ;
Milbrandt, J .
SCIENCE, 2004, 305 (5686) :1010-1013
[6]   CHD7 cooperates with PBAF to control multipotent neural crest formation [J].
Bajpai, Ruchi ;
Chen, Denise A. ;
Rada-Iglesias, Alvaro ;
Zhang, Junmei ;
Xiong, Yiqin ;
Helms, Jill ;
Chang, Ching-Pin ;
Zhao, Yingming ;
Swigut, Tomek ;
Wysocka, Joanna .
NATURE, 2010, 463 (7283) :958-U135
[7]   INO80 subfamily of chromatin remodeling complexes [J].
Bao, Yunhe ;
Shen, Xuetong .
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 2007, 618 (1-2) :18-29
[8]   PARP inhibition delays transition of hypertensive cardiopathy to heart failure in spontaneously hypertensive rats [J].
Bartha, Eva ;
Solti, Izabella ;
Kereskai, Laszlo ;
Lantos, Janos ;
Plozer, Eniko ;
Magyar, Klara ;
Szabados, Eszter ;
Kalai, Tamas ;
Hideg, Kalman ;
Halmosi, Robert ;
Sumegi, Balazs ;
Toth, Kalman .
CARDIOVASCULAR RESEARCH, 2009, 83 (03) :501-510
[9]   The etiology of Wolf-Hirschhorn syndrome [J].
Bergemann, AD ;
Cole, F ;
Hirschhorn, K .
TRENDS IN GENETICS, 2005, 21 (03) :188-195
[10]   Cardiac septal and valvular dysmorphogenesis in mice heterozygous for mutations in the homeobox gene Nkx2-5 [J].
Biben, C ;
Weber, R ;
Kesteven, S ;
Stanley, E ;
McDonald, L ;
Elliott, DA ;
Barnett, L ;
Köentgen, F ;
Robb, L ;
Feneley, M ;
Harvey, RP .
CIRCULATION RESEARCH, 2000, 87 (10) :888-895
12345678910