Small changes can make a big difference - MicroRNA regulation of cardiac hypertrophy

被引:56
作者
Gladka, Monika M. [1 ]
Martins, Paula A. da Costa [1 ]
de Windt, Leon J. [1 ]
机构
[1] Maastricht Univ, Dept Cardiol, Cardiovasc Res Inst, Fac Hlth Med & Life Sci, Maastricht, Netherlands
关键词
Cardiac hypertrophy; MicroRNA; Gene expression; Posttranscriptional regulation; Signaling; GENE-EXPRESSION; HEART; CALCINEURIN; CARDIOMYOCYTE; MYOCARDIN; DICER; MIR-21; DYSREGULATION; REVEALS; STRESS;
D O I
10.1016/j.yjmcc.2011.09.015
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cardiac hypertrophy is a thickening of the heart muscle that results in enlargement of the ventricles, which is the primary response of the myocardium to stress or mechanical overload. Cardiac pathological and physiological hemodynamic overload causes enhanced protein synthesis, sarcomeric reorganization and density, and increased cardiomyocyte size, all culminating into structural remodeling of the heart. With clinical evidence demonstrating that sustained hypertrophy is a key risk factor in heart failure development, much effort is centered on the identification of signals and pathways leading to pathological hypertrophy for future rational drug design in heart failure therapy. A wide variety of studies indicate that individual microRNAs exhibit altered expression profiles under experimental and clinical conditions of cardiac hypertrophy and heart failure. Here we review the recent literature, illustrating how single microRNAs regulate cardiac hypertrophy by classifying them by their prohypertrophic or antihypertrophic properties and their specific effects on intracellular signaling cascades, ubiquitination processes, sarcomere composition and by promoting inter-cellular communication. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:74 / 82
页数:9
相关论文
共 77 条
[31]   microRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart [J].
Liu, Ning ;
Bezprozvannaya, Svetlana ;
Williams, Andrew H. ;
Qi, Xiaoxia ;
Richardson, James A. ;
Bassel-Duby, Rhonda ;
Olson, Eric N. .
GENES & DEVELOPMENT, 2008, 22 (23) :3242-3254
[32]   MicroRNA Regulation in Cardiovascular Disease [J].
Martins, P. A. da Costa ;
Leptidis, S. ;
Salic, K. ;
De Windt, L. J. .
CURRENT DRUG TARGETS, 2010, 11 (08) :900-906
[33]   Conditional Dicer gene deletion in the postnatal myocardium provokes spontaneous cardiac remodeling [J].
Martins, Paula A. da Costa ;
Bourajjaj, Meriem ;
Gladka, Monika ;
Kortland, Mara ;
van Oort, Ralph J. ;
Pinto, Yigal M. ;
Molkentin, Jeffery D. ;
De Windt, Leon J. .
CIRCULATION, 2008, 118 (15) :1567-1576
[34]   MicroRNA-199b targets the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signalling [J].
Martins, Paula A. da Costa ;
Salic, Kanita ;
Gladka, Monika M. ;
Armand, Anne-Sophie ;
Leptidis, Stefanos ;
el Azzouzit, Hamid ;
Hansen, Arne ;
Coenen-de Roo, Christina J. ;
Bierhuizen, Marti F. ;
van der Nagel, Roel ;
van Kuik, Joyce ;
de Weger, Roel ;
de Bruin, Alain ;
Condorelli, Gianluigi ;
Arbones, Maria L. ;
Eschenhagen, Thomas ;
De Windt, Leon J. .
NATURE CELL BIOLOGY, 2010, 12 (12) :1220-U231
[35]   miR-21: a miRaculous Socratic paradox [J].
Martins, Paula A. da Costa ;
De Windt, Leon J. .
CARDIOVASCULAR RESEARCH, 2010, 87 (03) :397-400
[36]   MicroRNA-206: The skeletal muscle-specific myomiR [J].
McCarthy, John J. .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS, 2008, 1779 (11) :682-691
[37]   Left ventricular hypertrophy: A shift in paradigm [J].
Meijs, M. F. L. ;
de Windt, L. J. ;
de Jonge, N. ;
Cramer, M. -J. M. ;
Bots, M. L. ;
Mali, W. P. Th. M. ;
Doevendans, P. A. .
CURRENT MEDICINAL CHEMISTRY, 2007, 14 (02) :157-171
[38]   A calcineurin-dependent transcriptional pathway for cardiac hypertrophy [J].
Molkentin, JD ;
Lu, JR ;
Antos, CL ;
Markham, B ;
Richardson, J ;
Robbins, J ;
Grant, SR ;
Olson, EN .
CELL, 1998, 93 (02) :215-228
[39]  
Morkin E, 2000, MICROSC RES TECHNIQ, V50, P522, DOI 10.1002/1097-0029(20000915)50:6<522::AID-JEMT9>3.0.CO
[40]  
2-U