MicroRNAs-mediated epithelial-mesenchymal transition in fibrotic diseases

被引:58
|
作者
Zou, Xiao-Zhou [1 ]
Liu, Ting [1 ]
Gong, Zhi-Cheng [3 ]
Hu, Chang-Ping [1 ,2 ]
Zhang, Zheng [1 ,2 ]
机构
[1] Cent S Univ, Xiangya Sch Pharmaceut Sci, Dept Pharmacol, Changsha 410078, Hunan, Peoples R China
[2] Cent S Univ, Hunan Prov Key Lab Cardiovasc Res, Changsha 410078, Hunan, Peoples R China
[3] Cent S Univ, Xiangya Hosp, Dept Pharm, Changsha 410008, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
MicroRNAs; Epithelial-mesenchymal transition; Fibrotic diseases; IDIOPATHIC PULMONARY-FIBROSIS; GROWTH-FACTOR-BETA; SALVIANOLIC ACID-B; HEPATIC STELLATE CELLS; PLURIPOTENT STEM-CELLS; E-CADHERIN EXPRESSION; BREAST-CANCER CELLS; TGF-BETA; RENAL FIBROSIS; DIABETIC-NEPHROPATHY;
D O I
10.1016/j.ejphar.2016.12.003
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
MicroRNAs (miRNAs), a large family of small and highly conserved non-coding RNAs, regulate gene expression through translational repression or mRNA degradation. Aberrant expression of miRNAs underlies a spectrum of diseases including organ fibrosis. Recent evidence suggests that miRNAs contribute to organ fibrosis through mediating epithelial-mesenchymal transition (EMT). Alleviation of EMT has been proposed as a promising strategy against fibrotic diseases given the key role of EMT in fibrosis. miRNAs impact the expression of specific ligands, receptors, and signaling pathways, thus modulating EMT and consequently influencing fibrosis. This review summarizes the current knowledge concerning how miRNAs regulate EMT and highlights the specific roles that miRNAs-regulated EMT plays in fibrotic diseases as diverse as pulmonary fibrosis, hepatic fibrosis, renal fibrosis and cardiac fibrosis. It is desirable that a more comprehensive understanding of the functions of miRNAs-regulated EMT will facilitate the development of novel diagnostic and therapeutic strategies for various debilitating organ fibrosis.
引用
收藏
页码:190 / 206
页数:17
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