ArticleCytoJournal2026
Fat mass and obesity-associated gene overexpression ameliorates endothelial dysfunction after myocardial infarction by mediating N6-methyladenosine modification of ATP-binding cassette subfamily F member 1.
Article in CytoJournal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: Myocardial infarction (MI) is linked to high mortality, which highlights the need for early diagnosis and intervention to prevent heart failure. N6-methyladenosine (m6A) methylation of ribonucleic acid (RNA) influences endothelial dysfunction and MI. Here, the effects and associated mechanisms of fat mass and obesity-associated gene (FTO) on vascular endothelial cell (EC) function, as well as myocardial damage in mice following MI were investigated. Material and Methods: A human umbilical vein EC (HUVEC) model of oxygen-glucose deprivation (OGD) as well as a mouse MI model were used to detect MI-induced endothelial and myocardial damage. EC function was examined using cell-counting-kit-8, wound healing, migration, and tube formation assays. Methylated RNA immunoprecipitation (MeRIP) sequencing and RNA sequencing were utilized to analyze the m6A modifications and RNA expression patterns in control and FTO-overexpressing ECs following OGD. FTO and ATP-binding cassette subfamily F member 1 (ABCF1) levels were evaluated using western blotting. The relationship between FTO and ABCF1 was determined using RNA immunoprecipitation-quantitative polymerase chain reaction (RIPqPCR), MeRIP-qPCR, and RNA stability assays. Echocardiography and Masson's trichrome and hematoxylineosin staining were used to measure myocardial injury. Results: FTO expression was reduced in infarcted myocardial tissue and OGD-induced HUVECs ( Conclusion: Taken together, our study revealed that FTO overexpression restored OGD-induced endothelial dysfunction and myocardial pathological injury after MI. FTO increased ABCF1 expression in OGD-treated HUVECs through an m6A-dependent mechanism. These findings offer new insights into mitigating EC dysfunction and myocardial injury after MI.
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