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微小 RNA 在压力超负荷和缺血相关心肌重构中的作用。

Roles of microRNAs in pressure overload- and ischemia-related myocardial remodeling.

机构信息

The Cardiovascular Center, The First Hospital of Jilin University, Changchun, China; Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY, USA.

出版信息

Life Sci. 2013 Nov 26;93(23):855-62. doi: 10.1016/j.lfs.2013.08.023. Epub 2013 Sep 8.

Abstract

Cardiac remodeling, a term that spans maladaptation at the molecular, cellular, tissue and organ levels, is the key pathophysiological process that leads to heart failure (HF). In clinic, pressure overload and ischemia are the two most common reasons to induce cardiac remodeling and HF, which includes but is not limited to cardiac hypertrophy, fibrosis, and cardiomyocyte apoptosis. MicroRNAs (miRNAs) are endogenous, single-stranded, short non-coding RNAs. By imperfectly binding to the 3' untranslated region (UTR) of messenger RNAs (mRNAs), miRNAs are able to suppress target gene expression by promoting degradation or by inhibiting translation of the target mRNAs, thus playing an important role in a wide range of biologic processes. Growing evidence has indicated that miRNAs are aberrantly expressed in the cardiovascular system under experimental and clinical conditions with cardiac remodeling and HF. Clinically there is increasing evidence that miRNAs can act as diagnostic biomarker and even represent a novel therapeutic target in several cardiovascular disorders. This review provides an overview of several miRNAs' impacts in pressure-overload and ischemia-induced cardiac remodeling and HF.

摘要

心脏重构是一个涵盖分子、细胞、组织和器官水平适应不良的术语,是导致心力衰竭(HF)的关键病理生理过程。在临床上,压力超负荷和缺血是导致心脏重构和 HF 的两个最常见原因,其中包括但不限于心肌肥厚、纤维化和心肌细胞凋亡。微小 RNA(miRNAs)是内源性的、单链、短的非编码 RNA。通过与信使 RNA(mRNA)的 3'非翻译区(UTR)不完全结合,miRNAs 通过促进靶基因 mRNA 的降解或抑制其翻译来抑制靶基因的表达,从而在广泛的生物学过程中发挥重要作用。越来越多的证据表明,miRNAs 在实验和临床心脏重构和 HF 条件下的心血管系统中表达异常。临床上越来越多的证据表明,miRNAs 可以作为诊断生物标志物,甚至在几种心血管疾病中代表一种新的治疗靶点。本综述概述了几种 miRNAs 在压力超负荷和缺血诱导的心脏重构和 HF 中的作用。

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