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000141698 1001_ $$0P:(DE-2719)2811247$$aBerulava, Tea$$b0$$eFirst author
000141698 245__ $$aChanges in m6A RNA methylation contribute to heart failure progression by modulating translation.
000141698 260__ $$aOxford$$bWiley$$c2020
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000141698 520__ $$aDeregulation of epigenetic processes and aberrant gene expression are important mechanisms in heart failure. Here we studied the potential relevance of m6A RNA methylation in heart failure development.We analysed m6A RNA methylation via next-generation sequencing. We found that approximately one quarter of the transcripts in the healthy mouse and human heart exhibit m6A RNA methylation. During progression to heart failure we observed that changes in m6A RNA methylation exceed changes in gene expression both in mouse and human. RNAs with altered m6A RNA methylation were mainly linked to metabolic and regulatory pathways, while changes in RNA expression level mainly represented changes in structural plasticity. Mechanistically, we could link m6A RNA methylation to altered RNA translation and protein production. Interestingly, differentially methylated but not differentially expressed RNAs showed differential polysomal occupancy, indicating transcription-independent modulation of translation. Furthermore, mice with a cardiomyocyte restricted knockout of the RNA demethylase Fto exhibited an impaired cardiac function compared to control mice.We could show that m6A landscape is altered in heart hypertrophy and heart failure. m6A RNA methylation changes lead to changes in protein abundance, unconnected to mRNA levels. This uncovers a new transcription-independent mechanisms of translation regulation. Therefore, our data suggest that modulation of epitranscriptomic processes such as m6A methylation might be an interesting target for therapeutic interventions.
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000141698 542__ $$2Crossref$$i2019-12-17$$uhttp://creativecommons.org/licenses/by-nc/4.0/
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000141698 650_2 $$2MeSH$$aAnimals
000141698 650_2 $$2MeSH$$aEpigenesis, Genetic
000141698 650_2 $$2MeSH$$aHeart Failure: genetics
000141698 650_2 $$2MeSH$$aMethylation
000141698 650_2 $$2MeSH$$aMice
000141698 650_2 $$2MeSH$$aRNA: genetics
000141698 650_2 $$2MeSH$$aRNA: metabolism
000141698 650_2 $$2MeSH$$aRNA, Messenger: genetics
000141698 7001_ $$0P:(DE-HGF)0$$aBuchholz, Eric$$b1
000141698 7001_ $$0P:(DE-2719)2811844$$aElerdashvili, Vakhtang$$b2
000141698 7001_ $$0P:(DE-2719)2811063$$aPena Centeno, Tonatiuh$$b3
000141698 7001_ $$0P:(DE-2719)2811643$$aIslam, Rezaul$$b4
000141698 7001_ $$0P:(DE-HGF)0$$aLbik, Dawid$$b5
000141698 7001_ $$0P:(DE-HGF)0$$aMohamed, Belal A$$b6
000141698 7001_ $$0P:(DE-HGF)0$$aRenner, Andre$$b7
000141698 7001_ $$0P:(DE-HGF)0$$avon Lewinski, Dirk$$b8
000141698 7001_ $$0P:(DE-HGF)0$$aSacherer, Michael$$b9
000141698 7001_ $$0P:(DE-HGF)0$$aBohnsack, Katherine E$$b10
000141698 7001_ $$0P:(DE-HGF)0$$aBohnsack, Markus T$$b11
000141698 7001_ $$0P:(DE-2719)2811223$$aJain, Gaurav$$b12
000141698 7001_ $$0P:(DE-2719)2810626$$aCapece, Vincenzo$$b13
000141698 7001_ $$0P:(DE-2719)2812266$$aCleve, Nicole$$b14
000141698 7001_ $$0P:(DE-2719)2810773$$aBurkhardt, Susanne$$b15
000141698 7001_ $$0P:(DE-HGF)0$$aHasenfuss, Gerd$$b16
000141698 7001_ $$0P:(DE-2719)2000047$$aFischer, Andre$$b17$$eCorresponding author
000141698 7001_ $$0P:(DE-2719)9000440$$aToischer, Karl$$b18$$eLast author$$udzne
000141698 77318 $$2Crossref$$3journal-article$$a10.1002/ejhf.1672$$b : Wiley, 2019-12-17$$n1$$p54-66$$tEuropean Journal of Heart Failure$$v22$$x1388-9842$$y2019
000141698 773__ $$0PERI:(DE-600)1500332-2$$a10.1002/ejhf.1672$$gVol. 22, no. 1, p. 54 - 66$$n1$$p54-66$$tEuropean journal of heart failure$$v22$$x1388-9842$$y2020
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