ArticleApoptosis : an international journal on programmed cell death2025
The impact of YTHDF2-mediated NCOA4 methylation on myocardial ferroptosis.
Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- METTL3-mediated N6-methyladenosine modification ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Ferroptosis regulation in doxorubicin-induced cardiotoxicity: multi-mechanism interventions and translational strategies.Frontiers in pharmacology · 2026Review
- FTH1 mRNA-Protein Discordance in Cardiac Ferroptosis: Multilayer Posttranscriptional and Degradative Control.Cardiovascular therapeutics · 2026Review
- Exosomal lncRNA FENDRR Orchestrates Immune Remodelling and Ferroptosis in the Comorbidity of Lung Cancer and Type 1 Myocardial Infarction.Human mutation · 2026Article
- RSL3 promotes PARP1 apoptotic functions by distinct mechanisms during ferroptosis.Cellular & molecular biology letters · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The N6-Methyladenosine (m6A) modification is prevalent across various RNA species, including messenger RNAs (mRNAs) and long non-coding RNAs (lncRNAs), and has garnered significant interest due to its potential implications in cardiovascular disease. Despite extensive research, the precise relationship between m6A and myocardial infarction (MI) remains inadequately understood. The human YTH domain family 2 (YTHDF2) protein has emerged as a critical factor in this context, selectively recognizing m6A-modified RNAs and modulating their degradation. Our investigation revealed that the knockdown of YTHDF2 markedly enhanced ferroptosis in vitro, whereas the overexpression of YTHDF2 exhibited a significant protective effect. Mechanistically, it was elucidated that YTHDF2 suppresses the expression of nuclear receptor coactivator 4 (NCOA4) via m6A methylation. Furthermore, the inhibition of cardiomyocyte ferroptosis by YTHDF2 is contingent upon its regulation of NCOA4. Additionally, the enzyme methyltransferase-like 3 (METTL3) was identified as a pivotal factor in the m6A-mediated degradation of NCOA4 mRNA. Taken together, our results highlight the significant role of YTHDF2-mediated NCOA4 m6A methylation in the regulation of myocardial infarction and myocardial ferroptosis, suggesting that YTHDF2 may be a promising target for therapeutic interventions in myocardial infarction.
Indexed as
Identifiers
40167954What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.