Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands.
Cardiovasc Res. 2012 Mar 15;93(4):573-82. doi: 10.1093/cvr/cvr344. Epub 2011 Dec 16.
Multiple structural changes are known to occur in a failing heart. Myocyte hypertrophy, cardiomyocyte apoptosis, interstitial fibrosis, reduced capillary density, and activation of the immune system are all involved in the pathogenesis and progression of heart failure (HF). The molecular mechanisms underlying these changes of the myocardium have been extensively studied, and many pathways involved in these processes have been uncovered. Recently, it has become evident that a novel class of small non-coding RNAs, called miRNAs, also plays a key role in these structural changes of the heart. This review summarizes the current insights on the role of miRNAs outside myocytes in the heart. Specifically, we will discuss miRNA function in fibroblasts, endothelial cells and immune cells in response to myocardial stress as occurs after myocardial infarction and in the pathogenesis of HF.
已知在衰竭的心脏中会发生多种结构变化。心肌细胞肥大、心肌细胞凋亡、间质纤维化、毛细血管密度降低以及免疫系统的激活均参与心力衰竭（HF）的发病机制和进展。这些心肌变化的分子机制已被广泛研究，并且已经发现许多涉及这些过程的途径。最近，人们已经清楚地认识到，一类新的小非编码 RNA，称为 miRNAs，也在心脏的这些结构变化中发挥关键作用。这篇综述总结了目前关于 miRNA 在心肌细胞外的心脏中的作用的认识。具体来说，我们将讨论 miRNA 在心肌梗死后和 HF 发病机制中，在心外膜细胞、内皮细胞和免疫细胞中对心肌应激的反应中的功能。
