Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao 266021, China.
State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
Nat Commun. 2015 Apr 10;6:6779. doi: 10.1038/ncomms7779.
The abnormal autophagy is associated with a variety of cardiovascular diseases. Long noncoding RNAs (lncRNAs) are emerging as new factors in gene regulation, but how lncRNAs operate in the regulation of autophagy in the heart is unclear. Here we report that a long noncoding RNA, named autophagy promoting factor (APF), can regulate autophagic cell death by targeting miR-188-3p and ATG7. The results show that miR-188-3p suppresses autophagy and myocardial infarction by targeting ATG7. Further, we find that APF lncRNA regulates miR-188-3p, and thus affects ATG7 expression, autophagic cell death and myocardial infarction. Our present study reveals a novel regulating model of autophagic programme, which comprises APF, miR-188-3p and ATG7 in the heart. Modulation of their levels may serve as potential targets and diagnostic tools for novel therapeutic strategies of myocardial infarction and heart failure.
异常自噬与多种心血管疾病有关。长链非编码 RNA（lncRNA）作为基因调控的新因素而崭露头角，但 lncRNA 如何在心脏自噬的调节中发挥作用尚不清楚。在这里，我们报告了一种长链非编码 RNA，命名为自噬促进因子（APF），可以通过靶向 miR-188-3p 和 ATG7 来调节自噬性细胞死亡。结果表明，miR-188-3p 通过靶向 ATG7 抑制自噬和心肌梗死。此外，我们发现 APF lncRNA 调节 miR-188-3p，从而影响 ATG7 表达、自噬性细胞死亡和心肌梗死。本研究揭示了心脏中包含 APF、miR-188-3p 和 ATG7 的自噬程序的新调节模型。它们水平的调节可能成为心肌梗死和心力衰竭新治疗策略的潜在靶点和诊断工具。
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