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Erschienen in: Current Heart Failure Reports 5/2020

19.08.2020 | Translational Research in Heart Failure (J Backs & M van den Hoogenhof, Section Editors)

Epitranscriptomics in the Heart: a Focus on m6A

verfasst von: Jacob Z. Longenecker, Christopher J. Gilbert, Volha A. Golubeva, Colton R. Martens, Federica Accornero

Erschienen in: Current Heart Failure Reports | Ausgabe 5/2020

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Abstract

Purpose of Review

Post-transcriptional modifications are key regulators of gene expression that allow the cell to respond to environmental stimuli. The most abundant internal mRNA modification is N6-methyladenosine (m6A), which has been shown to be involved in the regulation of RNA splicing, localization, translation, and decay. It has also been implicated in a wide range of diseases, and here, we review recent evidence of m6A’s involvement in cardiac pathologies and processes.

Recent Findings

Studies have primarily relied on gain and loss of function models for the enzymes responsible for adding and removing the m6A modification. Results have revealed a multifaceted role for m6A in the heart’s response to myocardial infarction, pressure overload, and ischemia/reperfusion injuries. Genome-wide analyses of mRNAs that are differentially methylated during cardiac stress have highlighted the importance of m6A in regulating the translation of specific categories of transcripts implicated in pathways such as calcium handling, cell growth, autophagy, and adrenergic signaling in cardiomyocytes.

Summary

Regulation of gene expression by m6A is critical for cardiomyocyte homeostasis and stress responses, suggesting a key role for this modification in cardiac pathophysiology.
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Metadaten
Titel
Epitranscriptomics in the Heart: a Focus on m6A
verfasst von
Jacob Z. Longenecker
Christopher J. Gilbert
Volha A. Golubeva
Colton R. Martens
Federica Accornero
Publikationsdatum
19.08.2020
Verlag
Springer US
Erschienen in
Current Heart Failure Reports / Ausgabe 5/2020
Print ISSN: 1546-9530
Elektronische ISSN: 1546-9549
DOI
https://doi.org/10.1007/s11897-020-00473-z

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