MicroRNAs in Heart Failure

Melman, Yonathan F.; Shah, Ravi; Das, Saumya

doi:10.1161/circheartfailure.113.000266

Cited by 99 publications

(60 citation statements)

References 110 publications

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“…The incidence of cardiac arrhythmia and heart failure continues to rapidly increase, leading to a growing epidemic which constitutes a serious financial burden for society (Chugh et al, 2014; Melman et al, 2014). Despite the standard therapeutic strategies to treat adverse cardiac remodeling that precedes the development of arrhythmia and overt heart failure, their prevalence is still increasing and their morbidity and mortality have not been largely improved (Melman et al, 2014; Sardar et al, 2014).…”

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confidence: 99%

A snapshot of genetic and epigenetic basis of arrhythmia and heart failure

et al. 2015

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confidence: 99%

A snapshot of genetic and epigenetic basis of arrhythmia and heart failure

et al. 2015

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“…During the past years, great efforts have been made to provide the novel insights into the molecular mechanisms for decoding heart failure. But more studies have focused on elucidating the molecular mechanism that involved in protein‐coding genes and miRNAs 39. With the rapid development of next‐generation sequencing, a new type of long non‐coding transcripts that termed lncRNAs and encompassed more than 200 nucleotides have been discovered.…”

Section: Discussionmentioning

confidence: 99%

Integrative analysis of competing endogenous RNA networks reveals the functional lncRNAs in heart failure

Fan

Gao

Chen

et al. 2018

J Cellular Molecular Medi

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Heart failure has become one of the top causes of death worldwide. It is increasing evidence that lncRNAs play important roles in the pathology processes of multiple cardiovascular diseases. Additionally, lncRNAs can function as ceRNAs by sponging miRNAs to affect the expression level of mRNAs, implicating in numerous biological processes. However, the functional roles and regulatory mechanisms of lncRNAs in heart failure are still unclear. In our study, we constructed a heart failure‐related lncRNA‐mRNA network by integrating probe re‐annotation pipeline and miRNA‐target interactions. Firstly, some lncRNAs that had the central topological features were found in the heart failure‐related lncRNA‐mRNA network. Then, the lncRNA‐associated functional modules were identified from the network, using bidirectional hierarchical clustering. Some lncRNAs that involved in modules were demonstrated to be enriched in many heart failure‐related pathways. To investigate the role of lncRNA‐associated ceRNA crosstalks in certain disease or physiological status, we further identified the lncRNA‐associated dysregulated ceRNA interactions. And we also performed a random walk algorithm to identify more heart failure‐related lncRNAs. All these lncRNAs were verified to show a strong diagnosis power for heart failure. These results will help us to understand the mechanism of lncRNAs in heart failure and provide novel lncRNAs as candidate diagnostic biomarkers or potential therapeutic targets.

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“…Accumulated evidence has demonstrated that miRNA is closely associated with the initiation and progression of cardiomyocyte hypertrophy (3). miR-1 has been demonstrated to suppress cardiac hypertrophy by decreasing the expression levels of calmodulin and Mef2a (4).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-1 suppresses cardiac hypertrophy by targeting nuclear factor of activated T cells cytoplasmic 3

Yin

Zhao

Zhang

et al. 2012

Molecular Medicine Reports

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Abstract. Cardiomyocyte hypertrophy is a threat to human health due to the probability of sudden heart failure-induced mortality. Previous studies have demonstrated that nuclear factor of activated T cells cytoplasmic 3 (NFATC3) is important in the process of cardiomyocyte hypertrophy. However, the molecular mechanism underlying the alteration in the expression levels of NFATC3 during cardiomyocyte hypertrophy has remained to be fully elucidated. In order to shed light on the molecular mechanism, the present study employed several approaches, including the measurement of the cell surface area, analysis of the protein/DNA ratio, western blot analysis and a Luciferase reporter assay using isolated rat cardiomyocytes as model. The results showed that expression of microRNA-1 (miR-1) was reduced in patients diagnosed with cardiac hypertrophy and rat cardiomyocytes treated with pro-hypertrophic stimuli. The increase in the expression of miR-1 was able to inhibit the hypertrophic remodeling of cardiomyocytes. The suppression of miR-1 was sufficient to induce cardiomyocyte hypertrophy, and further experiments confirmed that NFATC3 was a target of miR-1 in cardiomyocytes. Forced expression of NFATC3 inhibited the protective activity of miR-1 against hypertrophic stimuli in the cardiomyocytes. These findings provided clarification of the regulatory signaling pathway underlying cardiac hypertrophy, and provided evidence that targeting the miR-1/NFATC3 pathway may be a promising strategy for the prevention and treatment of heart hypertrophy.

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MicroRNAs in Heart Failure

Cited by 99 publications

References 110 publications

A snapshot of genetic and epigenetic basis of arrhythmia and heart failure

A snapshot of genetic and epigenetic basis of arrhythmia and heart failure

Integrative analysis of competing endogenous RNA networks reveals the functional lncRNAs in heart failure

MicroRNA-1 suppresses cardiac hypertrophy by targeting nuclear factor of activated T cells cytoplasmic 3

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