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  • Review Article
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MicroRNAs in myocardial infarction

Nature Reviews Cardiology volume 12, pages 135–142 (2015)Cite this article

Subjects

Key Points

  • Tissue injury and inflammation regulate microRNAs in the heart after myocardial infarction

  • MicroRNAs control many processes in the infarcted heart, such as cardiomyocyte cell death and proliferation, neovascularization, and progenitor-cell-mediated repair

  • Acute inhibition or overexpression of microRNAs after myocardial infarction might be useful to limit tissue injury and improve neovascularization to prevent long-term negative remodelling and heart failure

  • Using microRNAs to induce cardiac regeneration by direct cardiac reprogramming of fibroblasts or by inducing cardiomyocyte proliferation offers new therapeutic opportunities

Abstract

MicroRNAs (miRNAs) are small noncoding RNAs that block translation or induce degradation of mRNA and thereby control patterns of gene expression. Acute myocardial infarction is a common cardiovascular event that results in cardiac remodelling and can consequently lead to the development of chronic heart failure. Several miRNAs have been shown to control important processes that contribute to the pathophysiological consequences of acute myocardial infarction. miRNAs can either promote or inhibit cardiomyocyte cell death, and also regulate postischaemic neovascularization. Cardiac regeneration can also be regulated by miRNAs that control cardiomyocyte proliferation or interfere with cardioprotective effects mediated by stem or progenitor cells. miRNAs can also be used for direct reprogramming of cardiac fibroblasts into cardiomyocytes. In this Review, we focus on the current understanding of the role of miRNAs in these processes, and particularly discuss the therapeutic potential of miRNAs in treating acute myocardial infarction.

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Figure 1: MicroRNAs regulate cardiomyocyte survival and proliferation.
Figure 2: MicroRNAs regulate angiogenesis.
Figure 3: MicroRNAs control the function of stem and progenitor cells and are used for intercellular communication.

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Acknowledgements

The authors are funded by the German Center for Cardiovascular Research DZHK (BMBF), the LOEWE Center for Cell and Gene Therapy (State of Hessen), the Deutsche Forschungsgemeinschaft (SFB834), and the Fondation Leducq Transatlantic Network 'MIRVAD'.

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  1. Institute for Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, Frankfurt am Main, 60590, Germany

    Reinier A. Boon & Stefanie Dimmeler

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Both authors researched data for the article, discussed its content, and wrote, reviewed, and edited the manuscript before submission.

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Correspondence to Stefanie Dimmeler.

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Competing interests

S.D. is an advisor for miRagen Therapeutics, and owns a patent on the development of miR 92a therapeutics. S.D. and R.A.B. are inventors on a patent on the development of miR 34a inhibitors for the treatment of cardiovascular disease.

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Boon, R., Dimmeler, S. MicroRNAs in myocardial infarction. Nat Rev Cardiol 12, 135–142 (2015). https://doi.org/10.1038/nrcardio.2014.207

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