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m6A RNA methylation in heart development, regeneration and disease

Hypertension Research volume 44, pages 1236–1237 (2021)Cite this article

Heart development is a complex process that requires the precise specification, proliferation, differentiation and maturation of cardiomyocytes. Heart failure (HF), a complex syndrome, is the leading cause of morbidity, mortality and economic burden around the world [1, 2]. Clinical aspects and current therapeutic approaches have resulted in limited success in the treatment of HF. Therefore, a new paradigm is needed based on better characterization of HF for novel clinical discoveries.

A number of studies have identified networks of genes and epigenetic marks that play important roles in embryonic heart development [4]. Importantly, recent studies have demonstrated that epitranscriptomic modifications, specifically m6A methylation, also play a vital role in cardiac gene expression, cardiomyocyte proliferation and heart regeneration [1, 2] (Fig. 1). Han et al. reported the potential involvement of m6A and its regulators in the regulation of cardiomyocytes (CMs) proliferation and cardiac regeneration [1]. These findings suggest the vital role of m6A and its regulators in the regulation of CMs proliferation and highlight a novel potential therapeutic strategy for cardiac regeneration.

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Fig. 1

References

  1. Han Z, Wang X, Xu Z, Cao Y, Gong R, Yu Y, et al. ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1. Theranostics. 2021;11:3000–16.

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  1. Cellular and Molecular Research Centre, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University, Chennai, India

    Arumugam Paramasivam & Jayaseelan Vijayashree Priyadharsini

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  1. Arumugam Paramasivam
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  2. Jayaseelan Vijayashree Priyadharsini
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Correspondence to Arumugam Paramasivam.

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Paramasivam, A., Priyadharsini, J.V. m6A RNA methylation in heart development, regeneration and disease. Hypertens Res 44, 1236–1237 (2021). https://doi.org/10.1038/s41440-021-00696-0

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