Macro advances in microRNAs and myocardial regeneration.
Macro advances in microRNAs and myocardial regeneration.
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DOI：
10.1097/hco.0000000000000050
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发表时间：
2014-05
影响因子：
2.3
通讯作者：
Martin JF
中科院分区：
文献类型：
--
作者：
Wang J;Martin JF
心肌损伤和疾病常常导致心力衰竭，这是全世界死亡的主要原因。为了实现心肌再生和促进心脏损伤有效治疗的发展，有必要揭示促进心肌再生的分子机制。本文就小分子非编码rna microRNAs在心肌再生中的作用的最新研究进展作一综述。心脏再生的研究取得了可喜的进展。一些mir，包括miR-590、miR-199a、miR-17-92簇、miR-199a-214簇、miR-34a和miR-15家族，最近被证明通过调节心脏修复过程中的不同过程，包括细胞死亡、增殖和代谢，在心肌再生中发挥重要作用。例如，miR-590通过激活心肌细胞增殖促进心脏再生，而miR-34a通过诱导细胞凋亡抑制心脏修复。这些最新的发现揭示了我们对心肌再生的理解，并提出了治疗心脏病的潜在新治疗靶点。
Myocardial injury and disease often results in heart failure, the leading cause of death worldwide. To achieve myocardial regeneration and foster development of efficient therapeutics for cardiac injury, it is essential to uncover molecular mechanisms that will promote myocardial regeneration. In this review, we examine the latest progress made in elucidation of the roles of small non coding RNAs called microRNAs (miRs) in myocardial regeneration. Promising progress has been made in studying cardiac regeneration. Several miRs, which includes miR-590, miR-199a, miR-17-92 cluster, miR-199a-214 cluster, miR-34a, and miR-15 family, have been recently shown to play an essential role in myocardial regeneration by regulating different processes during cardiac repair, including cell death, proliferation and metabolism. For example, miR-590 promotes cardiac regeneration through activating cardiomyocytes proliferation, while miR-34a inhibits cardiac repair through inducing apoptosis. These recent findings shed new light on our understanding of myocardial regeneration and suggest potential novel therapeutic targets to treat cardiac disease.