MicroRNA-21 in Cardiovascular Disease

被引:329
作者
Cheng, Yunhui [1 ,2 ]
Zhang, Chunxiang [1 ,2 ]
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Anesthesiol, RNA, Newark, NJ 07101 USA
[2] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Anesthesiol, Cardiovasc Res Lab, Newark, NJ 07101 USA
基金
美国国家卫生研究院;
关键词
MicroRNA; MicroRNA-21; Gene Expression; Cardiovascular Disease; MATRIX METALLOPROTEINASE-2; GENE-EXPRESSION; HUMAN HEART; MIR-21; IDENTIFICATION; INVOLVEMENT; SIGNATURE; PATTERN; TARGETS; PLAY;
D O I
10.1007/s12265-010-9169-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
MicroRNA-21 (miR-21) is a highly expressed microRNA (miRNA) in cardiovascular system. Recent studies have revealed that its expression is deregulated in heart and vasculature under cardiovascular disease conditions such as proliferative vascular disease, cardiac hypertrophy and heart failure, and ischemic heart disease. miR-21 is found to play important roles in vascular smooth muscle cell proliferation and apoptosis, cardiac cell growth and death, and cardiac fibroblast functions. Accordingly, miR-21 is proven to be involved in the pathogenesis of the above-mentioned cardiovascular diseases as demonstrated by both loss-of-function and gain-of-function approaches. Programmed cell death 4 (PDCD4), phosphatase and tensin homology deleted from chromosome 10 (PTEN), sprouty1 (SPRY1), and sprouty2 (SPRY2) are the current identified target genes of miR-21 that are involved in miR-21-mediated cardiovascular effects. miR-21 might be a novel therapeutic target in cardiovascular diseases. This review article summarizes the research progress regarding the roles of miR-21 in cardiovascular disease.
引用
收藏
页码:251 / 255
页数:5
相关论文
共 46 条
[1]   MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[2]   Identification of hundreds of conserved and nonconserved human microRNAs [J].
Bentwich, I ;
Avniel, A ;
Karov, Y ;
Aharonov, R ;
Gilad, S ;
Barad, O ;
Barzilai, A ;
Einat, P ;
Einav, U ;
Meiri, E ;
Sharon, E ;
Spector, Y ;
Bentwich, Z .
NATURE GENETICS, 2005, 37 (07) :766-770
[3]   MicroRNA-133 controls cardiac hypertrophy [J].
Care, Alessandra ;
Catalucci, Daniele ;
Felicetti, Federica ;
Bonci, Desiree ;
Addario, Antonio ;
Gallo, Paolo ;
Bang, Marie-Louise ;
Segnalini, Patrizia ;
Gu, Yusu ;
Dalton, Nancy D. ;
Elia, Leonardo ;
Latronico, Michael V. G. ;
Hoydal, Morten ;
Autore, Camillo ;
Russo, Matteo A. ;
Dorn, Gerald W., II ;
Ellingsen, Oyvind ;
Ruiz-Lozano, Pilar ;
Peterson, Kirk L. ;
Croce, Carlo M. ;
Peschle, Cesare ;
Condorelli, Gianluigi .
NATURE MEDICINE, 2007, 13 (05) :613-618
[4]   Antisense inhibition of human miRNAs and indications for an involvement of miRNA in cell growth and apoptosis [J].
Cheng, AM ;
Byrom, MW ;
Shelton, J ;
Ford, LP .
NUCLEIC ACIDS RESEARCH, 2005, 33 (04) :1290-1297
[5]   MicroRNAs are aberrantly expressed in hypertrophic heart - Do they play a role in cardiac hypertrophy? [J].
Cheng, Yunhui ;
Ji, Ruirui ;
Yue, Junming ;
Yang, Jian ;
Liu, Xiaojun ;
Chen, He ;
Dean, David B. ;
Zhang, Chunxiang .
AMERICAN JOURNAL OF PATHOLOGY, 2007, 170 (06) :1831-1840
[6]   MicroRNA-21 protects against the H2O2-induced injury on cardiac myocytes via its target gene PDCD4 [J].
Cheng, Yunhui ;
Liu, Xiaojun ;
Zhang, Shuo ;
Lin, Ying ;
Yang, Jian ;
Zhang, Chunxiang .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2009, 47 (01) :5-14
[7]   miR-145 and miR-143 regulate smooth muscle cell fate and plasticity [J].
Cordes, Kimberly R. ;
Sheehy, Neil T. ;
White, Mark P. ;
Berry, Emily C. ;
Morton, Sarah U. ;
Muth, Alecia N. ;
Lee, Ting-Hein ;
Miano, Joseph M. ;
Ivey, Kathryn N. ;
Srivastava, Deepak .
NATURE, 2009, 460 (7256) :705-U80
[8]   MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction [J].
Dong, Shimin ;
Cheng, Yunhui ;
Yang, Jian ;
Li, Jingyuan ;
Liu, Xiaojun ;
Wang, Xiaobin ;
Wang, Dong ;
Krall, Thomas J. ;
Delphin, Ellise S. ;
Zhang, Chunxiang .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (43) :29514-29525
[9]  
Friedman JM, 2009, SWISS MED WKLY, V139, P466, DOI 10.4414/smw.2009.12794
[10]   miR-21 gene expression triggered by AP-1 is sustained through a double-negative feedback mechanism [J].
Fujita, Shuji ;
Ito, Taiji ;
Mizutani, Taketoshi ;
Minoguchi, Shigeru ;
Yamamichi, Nlobutake ;
Sakurai, Kouhei ;
Iba, Hlideo .
JOURNAL OF MOLECULAR BIOLOGY, 2008, 378 (03) :492-504