The long noncoding RNA expression profiles of paroxysmal atrial fibrillation identified by microarray analysis

Su, Ying; Long, Li; Zhao, Sheng; Yue, Yunan; Yang, Shui-Xiang

doi:10.1016/j.gene.2017.11.025

Cited by 30 publications

(25 citation statements)

References 37 publications

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“…The lncRNA-mRNA regulatory network was constructed as described previously (also see details in the Supplementary material online ). 16 , 17 …”

Section: Methodsmentioning

confidence: 99%

Loss of AZIN2 splice variant facilitates endogenous cardiac regeneration

Wang

et al. 2018

Cardiovascular Research

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AimsLong noncoding RNAs (lncRNAs) are critical regulators of cardiovascular lineage commitment and heart wall development, but their roles in regulating endogenous cardiac regeneration are unclear. The present study investigated the role of human-derived lncRNA in regulating endogenous cardiac regeneration as well as the underlying mechanisms.Methods and resultsWe compared RNA sequencing data from human foetal and adult hearts and identified a novel lncRNA that was upregulated in adult hearts (Genesymbol NONHSAG000971/NONHSAT002258 or ENST00000497710.5), which was a splice variant of the AZIN2 gene (AZIN2-sv). We used quantitative PCR to confirm the increased expression of AZIN2-sv in adult rat hearts. Coexpression network analysis indicated that AZIN2-sv could regulate proliferation. Loss- and gain-of-function approaches demonstrated that AZIN2-sv negatively regulated endogenous cardiomyocyte proliferation in vitro and in vivo. Knockdown of AZIN2-sv attenuated ventricular remodelling and improved cardiac function after myocardial infarction. Phosphatase and tensin homolog (PTEN) was identified as a target of AZIN2-sv, their direct binding increased PTEN stability. Furthermore, AZIN2-sv acted as a microRNA-214 sponge to release PTEN, which blocked activation of the PI3 kinase/Akt pathway to inhibit cardiomyocyte proliferation.ConclusionsThe newly discovered AZIN2-sv suppressed endogenous cardiac regeneration by targeting the PTEN/Akt pathway. Thus, AZIN2-sv may be a novel therapeutic target for preventing and treating heart failure.

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“…The lncRNA-mRNA regulatory network was constructed as described previously (also see details in the Supplementary material online ). 16 , 17 …”

Section: Methodsmentioning

confidence: 99%

Loss of AZIN2 splice variant facilitates endogenous cardiac regeneration

Wang

et al. 2018

Cardiovascular Research

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“…Some of these studies were performed in lone AF patients [ 179 , 180 , 181 ], whereas in others valvular heart disease [ 177 ] or rheumatic valve disease [ 178 , 180 , 182 ] was also concurring. In most cases, either right or left atrial appendages were analysed [ 175 , 176 , 177 , 178 , 179 , 180 ], but in some cases right and left atrial samples were pooled together [ 179 , 180 , 181 ], while in other blood samples [ 180 , 183 ] or epicardial adipose tissue [ 184 , 185 ] were analysed. Given the wide variability of biological conditions studied, it is then not surprising that comparative analyses of these lncRNA transcriptomic analyses revealed no common AF signature [ 186 ].…”

Section: Epigenetics Of Atrial Fibrillationmentioning

confidence: 99%

Genetics and Epigenetics of Atrial Fibrillation

Lozano-Velasco

Franco

Aránega

et al. 2020

IJMS

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Atrial fibrillation (AF) is known to be the most common supraventricular arrhythmia affecting up to 1% of the general population. Its prevalence exponentially increases with age and could reach up to 8% in the elderly population. The management of AF is a complex issue that is addressed by extensive ongoing basic and clinical research. AF centers around different types of disturbances, including ion channel dysfunction, Ca2+-handling abnormalities, and structural remodeling. Genome-wide association studies (GWAS) have uncovered over 100 genetic loci associated with AF. Most of these loci point to ion channels, distinct cardiac-enriched transcription factors, as well as to other regulatory genes. Recently, the discovery of post-transcriptional regulatory mechanisms, involving non-coding RNAs (especially microRNAs), DNA methylation, and histone modification, has allowed to decipher how a normal heart develops and which modifications are involved in reshaping the processes leading to arrhythmias. This review aims to provide a current state of the field regarding the identification and functional characterization of AF-related epigenetic regulatory networks

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“…A number of reports have described differentially expressed lncRNAs in AF [ 12 , 13 , 136 , 137 ]. Mei et al [ 137 ] demonstrated that 182 lncRNAs were differentially expressed in left atrial tissue samples from patients with AF compared to patients with normal sinus rhythm.…”

Section: Lncrnas In Atrial Remodeling and Development Of Afmentioning

confidence: 99%

“…In past decade, the identification of lncRNAs opened a new avenue of investigation in AF research. Accumulating evidence shows that lncRNAs play key roles in several cardiovascular diseases, including AF [ 12 ]. Consequently, it is important to determine how they function in AF development and whether they could be used to treat AF.…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNAs in Atrial Fibrillation: Pluripotent Stem Cell-Derived Cardiomyocytes as a Model System

Bektik

Cowan

Wang

2020

IJMS

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Atrial fibrillation (AF) is a type of sustained arrhythmia in humans often characterized by devastating alterations to the cardiac conduction system as well as the structure of the atria. AF can lead to decreased cardiac function, heart failure, and other complications. Long non-coding RNAs (lncRNAs) have been shown to play important roles in the cardiovascular system, including AF; however, a large group of lncRNAs is not conserved between mouse and human. Furthermore, AF has complex networks showing variations in mechanisms in different species, making it challenging to utilize conventional animal models to investigate the functional roles and potential therapeutic benefits of lncRNAs for AF. Fortunately, pluripotent stem cell (PSC)-derived cardiomyocytes (CMs) offer a reliable platform to study lncRNA functions in AF because of certain electrophysiological and molecular similarities with native human CMs. In this review, we first summarize the broad aspects of lncRNAs in various heart disease settings, then focus on their potential roles in AF development and pathophysiology. We also discuss current uses of PSCs in AF research and describe how these studies could be developed into novel therapeutics for AF and other cardiovascular diseases.

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The long noncoding RNA expression profiles of paroxysmal atrial fibrillation identified by microarray analysis

Cited by 30 publications

References 37 publications

Loss of AZIN2 splice variant facilitates endogenous cardiac regeneration

Loss of AZIN2 splice variant facilitates endogenous cardiac regeneration

Genetics and Epigenetics of Atrial Fibrillation

Long Non-Coding RNAs in Atrial Fibrillation: Pluripotent Stem Cell-Derived Cardiomyocytes as a Model System

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