The function of miRNA in cardiac hypertrophy
- PDF / 284,634 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 37 Downloads / 166 Views
Cellular and Molecular Life Sciences
MULTI-AUTHOR REVIEW
The function of miRNA in cardiac hypertrophy Jian Wang • Xiao Yang
Received: 8 August 2012 / Revised: 9 August 2012 / Accepted: 9 August 2012 / Published online: 25 August 2012 Ó The Author(s) 2012. This article is published with open access at Springerlink.com
Abstract Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to altered stress or injury. The cellular responses of cardiomyocytes and noncardiomyocytes to various signaling pathways should be tightly and delicately regulated to maintain cardiac homeostasis and prevent pathological cardiac hypertrophy. MicroRNAs (miRNAs) are endogenous, single-stranded, short non-coding RNAs that act as regulators of gene expression by promoting the degradation or inhibiting the translation of target mRNAs. Recent studies have revealed expression signatures of miRNAs associated with pathological cardiac hypertrophy and heart failure in humans and mouse models of heart diseases. Increasing evidence indicates that dysregulation of specific miRNAs could alter the cellular responses of cardiomyocytes and non-cardiomyocytes to specific signaling upon the pathological hemodynamic overload, leading to cardiac hypertrophy and heart failure. This review summarizes the cell-autonomous functions of cardiomyocyte miRNAs regulated by different pathways and the roles of non-cardiomyocyte miRNAs in cardiac hypertrophy. The therapeutic effects of a number of miRNAs in heart diseases are also discussed. Keywords miRNAs Cardiac hypertrophy Signaling pathway Therapeutic target
J. Wang X. Yang (&) State Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, 20 Dongdajie, 100071 Beijing, China e-mail: [email protected] X. Yang Model Organism Division, E-institutes of Shanghai Universities, Shanghai Jiao Tong University, 200240 Shanghai, China
Introduction The heart is the first organ to form, and becomes functional during vertebrate embryonic development. Embryonic myocardial precursor cells from different origins give rise to different cell types, including cardiac and smooth muscle cells, valvular pacemaker, and endothelial cells, which coordinately build a functional heart [1]. Once developed, the homeostasis of adult heart is maintained by dynamic remodeling in response to altered stress or injury. Upon various mechanical, hemodynamic, hormonal, and pathologic stimuli, the cardiomyocytes initiate a hypertrophic response triggered by a complex cascade of signaling pathways to adapt to stress and improve the function of heart [2]. Compared to the physiologic hypertrophy, which involves proportional increases in the length and width of cardiac myocytes, prolonged concentric or eccentric hypertrophy is usually associated with enhanced synthesis of proteins, assembly of sarcomeres, and both perivascular and interstitial fibrosis, increased expression of embryonic genes including natriuretic peptide and fetal contractile protein genes, and eventually leads t
Data Loading...
