ArticleHereditas2025
RBM15 promotes hypoxia/reoxygenation-induced ferroptosis in human cardiomyocytes by mediating m6A modification of ACSL4.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Isoquercitrin suppresses neuronal ferroptosis in ischemic stroke via SIRT1-mediated deacetylation of H3K9 at the RBM15 promoter.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Humanized hiPSC Platforms for I/R Injury: Advancing Toward Precision Cardioprotection.Cardiovascular therapeutics · 2026Review
- MiR-200a-3p protects against myocardial ischemia-reperfusion injury via KEAP1-NRF2 signaling.Frontiers in physiology · 2026Article
- Crosstalk between ferroptosis and miRNA in type 2 diabetes mellitus and possible therapeutic targeting.European journal of medical research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myocardial infarction (AMI) refers to the acute necrosis of part of the myocardium caused by persistent and severe myocardial ischemia. The aim of the study was to investigate the effect of RNA binding motif protein 15 (RBM15) and acyl-CoA synthetase long chain family member 4 (ACSL4) on ischemia/reperfusion (I/R)-induced ferroptosis of cardiomyocytes. METHODS AND
resultsAC16 cells were treated with hypoxia/reoxygenation (H/R) to establish an in vitro myocardial infarction cell model. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay were used to determine gene expression. Cell Counting Kit-8 (CCK-8) assay was conducted to investigate cell viability. Ferroptosis level was evaluated by commercial kits. N6-methyladenosine (m6A) level was examined by M6A quantification analysis. RNA immunoprecipitation (RIP) assay, methylated RNA Immunoprecipitation (meRIP) assay and dual-luciferase reporter assay were adopted to verify the combination between RBM15 and ACSL4. ACSL4 mRNA stability was analyzed by Actinomycin D treatment. RBM15 mRNA level was increased in AMI patients' serums and H/R-induced AC16 cells. Silencing of RBM15 promoted H/R-mediated AC16 cell viability and inhibited H/R-induced AC16 cell oxidative stress and ferroptosis. Moreover, it was demonstrated that RBM15 knockdown inhibited m6A modification of ACSL4 and suppressed the stability of ACSL4 mRNA. Furthermore, ACSL4 overexpression restored the effects of RNM15 silencing on H/R-induced AC16 cell oxidative injury and ferroptosis.
conclusionRBM15 silencing repressed H/R-induced ferroptosis in human cardiomyocytes through regulating m6A modification of ACSL4.
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.