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miR-133a 与心肌梗死

MicroRNA-133a and Myocardial Infarction.

机构信息

1 Department of Cardiology, Xiangya Hospital, Central South University, Changsha, PR China.

2 Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA.

出版信息

Cell Transplant. 2019 Jul;28(7):831-838. doi: 10.1177/0963689719843806. Epub 2019 Apr 14.

DOI:10.1177/0963689719843806
PMID:30983393
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6719504/
Abstract

Myocardial infarction (MI) is the leading cause of morbidity and mortality in the world. The infarcted heart displays typical cell death cascades characterized by a loss of cells and fibrotic scarring in the myocardium. Cardiac hypertrophy and fibrosis largely contribute to ventricular wall thickening and stiffening, altogether defining an adverse cardiac remodeling that ultimately leads to impaired cardiac function and subsequent heart failure. Finding a strategy to promote therapeutic, instead of detrimental, cardiac remodeling may pose as a potent MI treatment. Accumulating evidence shows that microRNAs (miRNAs) may play an essential role in cardiovascular diseases. In particular, microRNA-133a (miR-133a) is one of the most abundant miRNAs in the heart. Multiple studies have demonstrated that miR-133a participates in the early pathology of MI, as well as in subsequent cardiac remodeling. In this review, we summarize recent research progress highlighting the regulatory effects of miR-133a in ischemic myocardial diseases, such as inhibiting angiogenesis, apoptosis, fibrosis, hypertrophy, and inflammation, while promoting therapeutic cardiac remodeling. The goal is to elicit a critical discussion on the translational direction of miRNA-mediated treatments towards a safe and effective MI therapy.

摘要

心肌梗死(MI)是世界上发病率和死亡率的主要原因。梗死的心脏显示出典型的细胞死亡级联,其特征是心肌细胞的丧失和纤维化瘢痕形成。心脏肥大和纤维化在很大程度上导致心室壁增厚和僵硬,共同定义了不良的心脏重构,最终导致心脏功能受损和随后的心力衰竭。寻找一种促进治疗性而非有害性心脏重构的策略可能是一种有效的 MI 治疗方法。越来越多的证据表明,microRNAs(miRNAs)可能在心血管疾病中发挥重要作用。特别是,microRNA-133a(miR-133a)是心脏中最丰富的 miRNAs 之一。多项研究表明,miR-133a 参与 MI 的早期病理,以及随后的心脏重构。在这篇综述中,我们总结了最近的研究进展,强调了 miR-133a 在缺血性心肌疾病中的调节作用,如抑制血管生成、细胞凋亡、纤维化、肥大和炎症,同时促进治疗性心脏重构。我们的目标是引发关于 miRNA 介导的治疗向安全有效的 MI 治疗的转化方向的关键讨论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/366f/6719504/0a9e8d919c22/10.1177_0963689719843806-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/366f/6719504/0a9e8d919c22/10.1177_0963689719843806-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/366f/6719504/0a9e8d919c22/10.1177_0963689719843806-fig1.jpg

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