LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription

Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and at...

Full description

Saved in:
Bibliographic Details
Published inNature communications Vol. 9; no. 1; p. 29
Main Authors Liu, Cui-Yun, Zhang, Yu-Hui, Li, Rui-Bei, Zhou, Lu-Yu, An, Tao, Zhang, Rong-Cheng, Zhai, Mei, Huang, Yan, Yan, Kao-Wen, Dong, Yan-Han, Ponnusamy, Murugavel, Shan, Chan, Xu, Sheng, Wang, Qi, Zhang, Yan-Hui, Zhang, Jian, Wang, Kun
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 02.01.2018
Nature Publishing Group
Nature Portfolio
Subjects
631/337/384
631/80/39
692/699/75
Attenuation
Autophagy
Biological activity
Biological effects
Cardiomyocytes
Cardiovascular diseases
Heart
Heart attacks
Heart diseases
Humanities and Social Sciences
Hydrogen peroxide
Ischemia
Medical treatment
multidisciplinary
Myocardial infarction
Myocardial ischemia
p53 Protein
Phagocytosis
Reperfusion
Science
Science (multidisciplinary)
Transcription
Online AccessGet full text

Cover

More Information
Summary:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H 2 O 2 and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases. Little is known about the role of long lncRNAs in autophagy. The authors identify lncCAIF, and show that it suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53 -mediated transcription of myocardin.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-017-02280-y