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本文引用的文献

1
Programmed necrosis, not apoptosis, in the heart.心肌程序性细胞坏死,而非细胞凋亡。
Circ Res. 2011 Apr 15;108(8):1017-36. doi: 10.1161/CIRCRESAHA.110.225730.
2
miR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytes.miR-24 抑制凋亡并抑制小鼠心肌细胞中的 Bim。
J Exp Med. 2011 Mar 14;208(3):549-60. doi: 10.1084/jem.20101547. Epub 2011 Mar 7.
3
miR-499 regulates mitochondrial dynamics by targeting calcineurin and dynamin-related protein-1.miR-499 通过靶向钙调神经磷酸酶和动力相关蛋白 1 调节线粒体动力学。
Nat Med. 2011 Jan;17(1):71-8. doi: 10.1038/nm.2282. Epub 2010 Dec 26.
4
Circulating MicroRNA-208b and MicroRNA-499 reflect myocardial damage in cardiovascular disease.循环中的微小RNA-208b和微小RNA-499反映心血管疾病中的心肌损伤。
Circ Cardiovasc Genet. 2010 Dec;3(6):499-506. doi: 10.1161/CIRCGENETICS.110.957415. Epub 2010 Oct 4.
5
Synergistic effects of the GATA-4-mediated miR-144/451 cluster in protection against simulated ischemia/reperfusion-induced cardiomyocyte death.GATA-4 介导的 miR-144/451 簇在防治模拟缺血/再灌注诱导的心肌细胞死亡中的协同作用。
J Mol Cell Cardiol. 2010 Nov;49(5):841-50. doi: 10.1016/j.yjmcc.2010.08.007. Epub 2010 Aug 11.
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Apolipoprotein B synthesis inhibition: results from clinical trials.载脂蛋白 B 合成抑制:临床试验结果。
Curr Opin Lipidol. 2010 Aug;21(4):319-23. doi: 10.1097/MOL.0b013e32833af4c1.
7
MicroRNA-21 is a downstream effector of AKT that mediates its antiapoptotic effects via suppression of Fas ligand.微小 RNA-21 是 AKT 的下游效应因子,通过抑制 Fas 配体来介导其抗细胞凋亡作用。
J Biol Chem. 2010 Jun 25;285(26):20281-90. doi: 10.1074/jbc.M110.109207. Epub 2010 Apr 19.
8
Efficacy and safety of mipomersen, an antisense inhibitor of apolipoprotein B, in hypercholesterolemic subjects receiving stable statin therapy.在接受稳定他汀类药物治疗的高胆固醇血症患者中,载脂蛋白 B 反义抑制剂米泊美生的疗效和安全性。
J Am Coll Cardiol. 2010 Apr 13;55(15):1611-8. doi: 10.1016/j.jacc.2009.11.069.
9
A translational study of circulating cell-free microRNA-1 in acute myocardial infarction.循环细胞游离 microRNA-1 在急性心肌梗死中的转化研究。
Clin Sci (Lond). 2010 Apr 20;119(2):87-95. doi: 10.1042/CS20090645.
10
Downregulation of microRNA-29 by antisense inhibitors and a PPAR-gamma agonist protects against myocardial ischaemia-reperfusion injury.反义抑制剂和过氧化物酶体增殖物激活受体-γ激动剂下调 microRNA-29 可保护心肌免受缺血再灌注损伤。
Cardiovasc Res. 2010 Aug 1;87(3):535-44. doi: 10.1093/cvr/cvq053. Epub 2010 Feb 17.

微小 RNA:心脏损伤与保护的新角色。

MicroRNAs: new players in cardiac injury and protection.

机构信息

Division of Cardiology, Virginia Commonwealth University, Richmond, VA 23298, USA.

出版信息

Mol Pharmacol. 2011 Oct;80(4):558-64. doi: 10.1124/mol.111.073528. Epub 2011 Jul 7.

DOI:10.1124/mol.111.073528
PMID:21737570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3187527/
Abstract

MicroRNAs (miRNAs) have emerged as a novel class of endogenous, small, noncoding RNAs that negatively regulate gene expression via degradation or translational inhibition of their target mRNAs. Over 700 miRNAs have been identified and sequenced in humans, and the number of miRNA genes is estimated at more than 1000. Individual miRNA is functionally important as a transcription factor because it has the ability to regulate the expression of multiple genes through binding to its target with imperfect or perfect complement. In the heart, miRNAs have been involved in several clinical scenarios, such as ischemia/reperfusion (I/R) injury and heart failure suggesting that regulation of their function could be used as a novel cardioprotective strategy. In particular, miRNA-1, miRNA-21, miRNA-24, miRNA-29, miRNA-92a, miRNA-126, miRNA-133, miRNA-320, miRNA-199a, miRNA-208, and miRNA-195 have been shown to be regulated after I/R injury. Because tissue miRNAs can be released into circulating blood, they also offer exciting new opportunities for developing sensitive biomarkers, including miRNA-1, miRNA-126, miR-208, and miRNA-499, for acute myocardial infarction and other cardiac diseases.

摘要

微小 RNA(miRNA)是一类新发现的内源性、小型、非编码 RNA,通过降解或翻译抑制靶 mRNA 来负调控基因表达。在人类中已鉴定和测序了超过 700 种 miRNA,miRNA 基因的数量估计超过 1000 个。单个 miRNA 作为转录因子具有重要的功能,因为它能够通过与靶标不完全或完全互补结合来调节多个基因的表达。在心脏中,miRNA 参与了几种临床情况,如缺血/再灌注(I/R)损伤和心力衰竭,表明调节其功能可以作为一种新的心脏保护策略。特别是,miRNA-1、miRNA-21、miRNA-24、miRNA-29、miRNA-92a、miRNA-126、miRNA-133、miRNA-320、miRNA-199a、miRNA-208 和 miRNA-195 在 I/R 损伤后被证明是受调控的。由于组织 miRNA 可以释放到循环血液中,因此它们也为开发敏感的生物标志物提供了令人兴奋的新机会,包括 miRNA-1、miRNA-126、miR-208 和 miRNA-499,用于急性心肌梗死和其他心脏疾病。