Regulation of N6-Methyladenosine after Myocardial Infarction

Mélanie Vausort, Magdalena Niedolistek, Andrew I. Lumley, Marta Oknińska, Aleksandra Paterek, Michał Mączewski, Xiangyi Dong, Christian Jäger, Carole L. Linster, Przemyslaw Leszek, Yvan Devaux*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

7 Citations (Scopus)


Development of heart failure (HF) after myocardial infarction (MI) is responsible for premature death. Complex cellular and molecular mechanisms are involved in this process. A number of studies have linked the epitranscriptomic RNA modification N6-methyladenosine (m6A) with HF, but it remains unknown how m6A affects the risk of developing HF after MI. We addressed the regulation of m6A and its demethylase fat mass and obesity-associated (FTO) after MI and their association with HF. Using liquid chromatography coupled to mass spectrometry, we observed an increase of m6A content in the infarcted area of rat hearts subjected to coronary ligation and a decrease in blood. FTO expression measured by quantitative PCR was downregulated in the infarcted hearts. In whole blood samples collected at the time of reperfusion in MI patients, m6A content was lower in patients who developed HF as attested by a 4-month ejection fraction (EF) of ≤40% as compared to patients who did not develop HF (EF > 50%). M6A content was higher in females. These results show that m6A measured in blood is associated with HF development after MI and motivate further investigation of the potential role of m6A as a novel epitranscriptomics biomarker and therapeutic target of HF.

Original languageEnglish
Article number2271
Issue number15
Publication statusPublished - 22 Jul 2022


  • biomarker
  • heart failure
  • m6A
  • myocardial infarction
  • RNA methylation


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