Regulation of fetal gene expression in heart failure

被引:216
作者
Dirkx, Ellen [1 ,2 ]
da Costa Martins, Paula A. [1 ]
De Windt, Leon J. [1 ]
机构
[1] Maastricht Univ, Fac Hlth Med & Life Sci, CARIM Sch Cardiovasc Dis, Dept Cardiol, Maastricht, Netherlands
[2] Royal Netherlands Acad Sci, ICIN Netherlands Heart Inst, Utrecht, Netherlands
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2013年 / 1832卷 / 12期
基金
欧洲研究理事会;
关键词
Gene regulation; Transcription factors; Epigenetics; SERUM RESPONSE FACTOR; CARDIAC TRANSCRIPTION FACTOR; ATRIAL SEPTAL-DEFECT; CALCINEURIN-INTERACTING PROTEIN-1; SINGLE-NUCLEOTIDE POLYMORPHISMS; LEFT-VENTRICULAR HYPERTROPHY; BONE MORPHOGENETIC PROTEIN; MYOCYTE ENHANCER FACTOR-2; II HISTONE DEACETYLASES; NATRIURETIC-FACTOR GENE;
D O I
10.1016/j.bbadis.2013.07.023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
During the processes leading to adverse cardiac remodeling and heart failure, cardiomyocytes react to neurohumoral stimuli and biomechanical stress by activating pathways that induce pathological hypertrophy. The gene expression patterns and molecular changes observed during cardiac hypertrophic remodeling bare resemblance to those observed during fetal cardiac development. The re-activation of fetal genes in the adult failing heart is a complex biological process that involves transcriptional, posttranscriptional and epigenetic regulation of the cardiac genome. In this review, the mechanistic actions of transcription factors, microRNAs and chromatin remodeling processes in regulating fetal gene expression in heart failure are discussed. (C) 2013 Elsevier B.V. All rights reserved.
引用
收藏
页码:2414 / 2424
页数:11
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