ArticleFrontiers in pharmacology2021
Aging-Associated Differences in Epitranscriptomic m6A Regulation in Response to Acute Cardiac Ischemia/Reperfusion Injury in Female Mice.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Emerging Dual Roles of ALKBH5 in Ischemia-reperfusion Injury: Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- The mechanism of m6A modification in cardiovascular diseases: A systematic review.Genes & diseases · 2026Review
- FTO in cardiovascular diseases: mechanisms, context dependence, and translational opportunities.Frontiers in cell and developmental biology · 2026Review
- The 6-methyladenine erasers ALKBH5 and FTO influence chemotherapy efficiency in bladder cancer cell lines.Annals of translational medicine · 2025Article
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- Comprehensive analysis of diagnostic biomarkers related to histone acetylation in acute myocardial infarction.BMC medical genomics · 2025Article
- N6-methyladenosine RNA landscape in the aged mouse hearts.Frontiers in cardiovascular medicine · 2025Article
- Article
- Unlocking the dark matter: noncoding RNAs and RNA modifications in cardiac aging.American journal of physiology. Heart and circulatory physiology · 2024Review
- METTL3 Mediates Microglial Activation and Blood-Brain Barrier Permeability in Cerebral Ischemic Stroke by Regulating NLRP3 Inflammasomes Through m6A Methylation Modification.Neurotoxicity research · 2024Article
- Aging-Associated ALKBH5-mJournal of the American Heart Association · 2024Article
- N6-methyladenosine (m6A) modification in inflammation: a bibliometric analysis and literature review.PeerJ · 2024Review
- FTO in health and disease.Frontiers in cell and developmental biology · 2024Review
- METTL3 Deficiency Aggravates Hepatic Ischemia/Reperfusion Injury in Mice by Activating the MAPK Signaling Pathway.International journal of medical sciences · 2024Article
- Key mBMC medical genomics · 2023Article
- RNA modification mEpigenetics · 2023Review
- Methylation across the central dogma in health and diseases: new therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases.Neurology international · 2023Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Elderly patients are more susceptible to ischemic injury. N6-methyladenosine (m6A) modification is the most abundant reversible epitranscriptomic modification in mammalian RNA and plays a vital role in many biological processes. However, it is unclear whether age difference impacts m6A RNA methylation in hearts and their response to acute myocardial ischemia/reperfusion (I/R) injury. In this study, we measured the global level of m6A RNA methylation as well as the expression of m6A RNA "writers" (methylation enzymes) and "erasers" (demethylation enzymes) in the hearts of young and elderly female mice undergone sham surgery or acute MI/R injury. We found that m6A RNA level and associate modifier gene expression was similar in intact young and old female hearts. However, young hearts show a significant reduction in m6A RNA while elderly hearts showed only a slight reduction in m6A RNA in response to acute I/R injury. To explore the mechanism of differential level of m6A RNA modification, we use qRT-PCR and Western blotting to compare the mRNA and protein expression of major m6A-related "writers" (Mettl3, Mettl14, and WTAP) and 'erasers" (ALKBH5 and FTO). Mettl3 mRNA and protein expression were significantly reduced in both young and elderly hearts. However, the levels of FTO's mRNA and protein were only significantly reduced in ischemic elderly hearts, and age-related downregulation of FTO may offset the effect of reduced Mettl3 on reduced m6A RNA level in the hearts of aging mice hearts with acute I/R injury, indicating aging-related differences in epitranscriptomic m6A regulation in hearts in response to acute I/R injury. To further investigate specific I/R related targets of Mettl3, we overexpressed Mettl3 in cardiomyocyte line (HL1) using lentiviral vector, and the m6A enrichment of Bcl2, Bax and PTEN were quantified with m6A RIP-qPCR, we found that m6A modification of PTEN mRNA decreased after
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.