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

Liu, Cui-Yun; Zhang, Yuhui; Li, Ruibei; Zhou, Luqian; An, Tao; Zhang, Rongcheng; Zhai, Mei; Huang, Yan; Ke, Yan; Dong, Yanhan; Ponnusamy, Murugavel; Shan, Chan; Xu, Sheng; Wang, Qi; Zhang, Yanhui; Zhang, Jian; Wang, Kun

doi:10.1038/s41467-017-02280-y

Cited by 265 publications

(197 citation statements)

References 44 publications

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“…Moreover, many lncRNAs have been found to be modulators in the progression of cardiovascular diseases (CVDs), such as cardiovascular aging, myocardial infarction and cardiac hypertrophy [34,35]. Moreover, several previous studies have reported that lncRNAs can regulate biological processes that are associated with myocardial infarction [36]. In our current study, we found that the relative expression of lncRNA SNHG8 was upregulated in AMI.…”

Section: Discussionsupporting

confidence: 53%

LncRNA SNHG8 is identified as a key regulator of acute myocardial infarction by RNA-seq analysis

et al. 2019

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BackgroundLong noncoding RNAs (lncRNAs) are involved in numerous physiological functions. However, their mechanisms in acute myocardial infarction (AMI) are not well understood.MethodsWe performed an RNA-seq analysis to explore the molecular mechanism of AMI by constructing a lncRNA-miRNA-mRNA axis based on the ceRNA hypothesis. The target microRNA data were used to design a global AMI triple network. Thereafter, a functional enrichment analysis and clustering topological analyses were conducted by using the triple network. The expression of lncRNA SNHG8, SOCS3 and ICAM1 was measured by qRT-PCR. The prognostic values of lncRNA SNHG8, SOCS3 and ICAM1 were evaluated using a receiver operating characteristic (ROC) curve.ResultsAn AMI lncRNA-miRNA-mRNA network was constructed that included two mRNAs, one miRNA and one lncRNA. After RT-PCR validation of lncRNA SNHG8, SOCS3 and ICAM1 between the AMI and normal samples, only lncRNA SNHG8 had significant diagnostic value for further analysis. The ROC curve showed that SNHG8 presented an AUC of 0.850, while the AUC of SOCS3 was 0.633 and that of ICAM1 was 0.594. After a pairwise comparison, we found that SNHG8 was statistically significant (P SNHG8-ICAM1 = 0.002; P SNHG8-SOCS3 = 0.031). The results of a functional enrichment analysis of the interacting genes and microRNAs showed that the shared lncRNA SNHG8 may be a new factor in AMI.ConclusionsOur investigation of the lncRNA-miRNA-mRNA regulatory networks in AMI revealed a novel lncRNA, lncRNA SNHG8, as a risk factor for AMI and expanded our understanding of the mechanisms involved in the pathogenesis of AMI.

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Section: Discussionsupporting

confidence: 53%

LncRNA SNHG8 is identified as a key regulator of acute myocardial infarction by RNA-seq analysis

et al. 2019

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“…For example, Li et al showed that lncRNA KCNQ1OT1 suppression protected against myocardial ischemia following acute MI [16]. Liu et al showed that lncRNA CAIF suppressed autophagy and attenuated MI through blocking p53-mediated myocardin transcription [17]. Zhang et al showed that lncRNA GAS5 regulated MI through regulating miR-525-5p/CALM2 axis [18].…”

Section: Discussionmentioning

confidence: 99%

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

2019

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This study is aimed to explore the roles of LINC00528 in myocardial infarction (MI) progression. Quantitative real-time PCR showed that the expression of LINC00528 and COX-2 was upregulated while miR-143-3p expression was down-regulated in post-MI cells. In function assays, LINC00528 suppression promoted post-MI cells proliferation and reduced cell apoptosis in vitro. In mechanism, LINC00528 interacted with miR-143-3p in post-MI cells. COX-2 served as a target of miR-143-3p in post-MI cells. Besides, LINC00528 inhibition on COX-2 expression and post-MI cells progression could be partially abolished by miR-143-3p inhibitors. Therefore, our findings suggested that LINC00528 exerted its regulatory roles in MI via the miR-143-3p/COX-2 axis, which provided a potential therapeutic target for MI patients treatment. ARTICLE HISTORY

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“…Studying the effects of lncRNAs on autophagy, Liu et al [50] found that the lncRNA cardiac autophagy inhibitory factor (CAIF) showed cardioprotective properties by interacting with p53 protein, thereby blocking it from activating myocardin transcription and subsequent cardiac autophagy.…”

Section: Lncrnas and Myocardial Infarctionmentioning

confidence: 99%

Expedition to the missing link: Long noncoding RNAs in cardiovascular diseases

Yeh

Chang

et al. 2020

J Biomed Sci

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With the advances in deep sequencing-based transcriptome profiling technology, it is now known that human genome is transcribed more pervasively than previously thought. Up to 90% of the human DNA is transcribed, and a large proportion of the human genome is transcribed as long noncoding RNAs (lncRNAs), a heterogenous group of non-coding transcripts longer than 200 nucleotides. Emerging evidence suggests that lncRNAs are functional and contribute to the complex regulatory networks involved in cardiovascular development and diseases. In this article, we will review recent evidence on the roles of lncRNAs in the biological processes of cardiovascular development and disorders. The potential applications of lncRNAs as biomarkers and targets for therapeutics are also discussed.

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

Cited by 265 publications

References 44 publications

LncRNA SNHG8 is identified as a key regulator of acute myocardial infarction by RNA-seq analysis

LncRNA SNHG8 is identified as a key regulator of acute myocardial infarction by RNA-seq analysis

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

Expedition to the missing link: Long noncoding RNAs in cardiovascular diseases

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