ArticleJournal of cardiothoracic surgery2025
YTHDF2 mediates the protective effects of MG53 on myocardial infarction injury via recognizing the m6A modification of MG53.
Article in Journal of cardiothoracic surgery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- OGT-mediated O-GlcNAcylation Protects Against Myocardial Ischemia-Reperfusion Injury via Targeting MG53.Applied biochemistry and biotechnology · 2026Article
- mRedox biology · 2026Review
- Decreased serum MG53 levels are associated with SHBG and androgen excess in women with polycystic ovary syndrome.Scientific reports · 2026Observational
- Lactate regulates the YTHDF2-FTH1 axis to promote cardiomyocyte ferroptosis and aggravate myocardial ischemia-reperfusion injury.Scientific reports · 2026Article
- mExperimental & molecular medicine · 2025Review
- Study on the mechanism and clinical value of miR-210-3p and miR-582-5p in acute myocardial infarction by targeting MXD1.Journal of cardiothoracic surgery · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
introductionHigh levels of MG53 may attenuate the damage from myocardial infarction (MI). Furthermore, N6-methyl-adenosine (m6A) methylation is a mode of RNA modification that influences mRNA functions. Whether m6A modification on MG53 exerts a protective role on myocardial injury remains largely unknown. MATERIALS AND
methodsWe established hypoxia/reoxygenation (H/R) H9c2 cell and myocardial ischemia reperfusion (I/R) rat models. MG53 expression was detected using RT-qPCR, and its m6A levels were measured using Me-RIP. The relationship between MG53 and YTHDF2 was evaluated using RNA immunoprecipitation, FISH and immunofluorescence assay, and luciferase reporter assay. MI area of rats was determined using TTC staining. Cell apoptosis was assessed by flow cytometry and TUNEL assay.
resultsThe m6A levels of MG53 were increased in H/R-induced H9c2 cells and the myocardium of I/R rats. Moreover, knockdown of YTHDF2 recognized the m6A modification of MG53 and enhanced MG53 stability. Overexpression of MG53 inhibited apoptosis of H/R-treated H9c2 cells, which was reversed by YTHDF2, while downregulation of MG53 m6A methylation caused by METTL3 knockdown further abrogated the effect induced by YTHDF2. Additionally, MG53 attenuated MI and apoptosis in I/R rats, which were rescued by YTHDF2.
conclusionYTHDF2 hinders the protective effect of MG53 on MI by recognizing the m6A modification of MG53.
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