ArticleMolecular medicine (Cambridge, Mass.)2024
FTO suppresses cardiac fibrosis after myocardial infarction via m
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Associations BetweenBiology · 2026Article
- IGF2BP3 promotes early angiogenesis in pulmonary fibrosis by stabilizing HIF-1α.Molecular and cellular biochemistry · 2026Article
- Vascular smooth muscle cell FTO deletion aggravates atherosclerotic plaque instability by promoting VSMC migration through the NScience China. Life sciences · 2026Article
- Review
- CircRNA-TMEM71 Inhibits Human Aortic Smooth Muscle Cell Ferroptosis and Prevents Aortic Dissection Formation Through IGF2BP3-Mediated Stability of FSP1.Journal of the American Heart Association · 2026Article
- FTO-Eci1 Axis Mediates Exercise-Induced Cardioprotection in Pressure Overload Mice.Biomolecules · 2026Article
- FTO in cardiovascular diseases: mechanisms, context dependence, and translational opportunities.Frontiers in cell and developmental biology · 2026Review
- Identification of FTO as a key m6A demethylase linking immune dysregulation to sepsis pathogenesis.Frontiers in immunology · 2026Article
- Integrative multi-omic profiling of the chronically hypoxic heart: focus on mFrontiers in cell and developmental biology · 2026Article
- M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.Redox report : communications in free radical research · 2025Article
- Hypoxia-mediated regulation of mRNA metabolism: from transcription to stability.Cell communication and signaling : CCS · 2025Review
- The Clinical Relevance of FTO as a Demethylase Beyond Cancer: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- Circular RNA circFTO promotes pressure overload-induced cardiac hypertrophy by encoding a novel protein FTO-36aa.Journal of thoracic disease · 2025Article
- Comprehensive Analysis of N6-Methyladenosine Methylation in Transverse Aortic Constriction-Induced Cardiac Fibrosis Based on MeRIP-Seq Analysis.Biomedicines · 2025Article
- Epitranscriptomic regulation of HIF-1: bidirectional regulatory pathways.Molecular medicine (Cambridge, Mass.) · 2025Review
- Epigenetic modifications in cardiac fibrosis: recent evidence of new pharmacological targets.Frontiers in molecular biosciences · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundCardiac fibrosis is common in myocardial infarction (MI), leading to progressive cardiac dysfunction. Studies suggested that the abnormal N
methodsWestern blot and quantitative real-time PCR were performed to detect the expression of FTO in the fibrotic tissue of rats. The functions of FTO on collagen biosynthesis were analyzed in vitro and in vivo. The underlying targets of FTO were selected through RNA-seq with m
resultsThe expression of FTO was decreased in the fibrotic tissue of post-infarction rats. The HIF-1 signal pathway was enriched after MI. HIF-1α could bind to the promoter of FTO and inhibit its expression. Functionally, FTO inhibited collagen synthesis after MI in vitro and in vivo. Mechanistically, EPRS was selected as the underlying target of FTO-induced m
conclusionsFTO, identified as a cardioprotective factor, suppressed collagen synthesis in post-infarction cardiac fibrosis via m
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