ArticleBiology direct2024
METTL3 mediates m6A modification of lncRNA CRNDE to promote ATG10 expression and improve brain ischemia/reperfusion injury through YTHDC1.
Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The role of N6-methyladenosine associated genes in ischemic stroke risk: interplay with environmental factors.Journal of thrombosis and thrombolysis · 2026Review
- Emerging Dual Roles of ALKBH5 in Ischemia-reperfusion Injury: Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- METTL7B-stabilized lncRNA-MIR22HG to drive p53-mediated neuronal apoptosis via the ubiquitinating JARID2 in cerebral ischemia/reperfusion injury.Cell biology and toxicology · 2026Article
- The spatiotemporal dynamic evolution of post-stroke neuroinflammation: energy metabolism mechanisms of acute response and chronic progression.Frontiers in pharmacology · 2026Review
- Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia.Molecular brain · 2025Article
- The role of m6A regulators mRNA expression in peripheral blood mononuclear cells in chronic hepatitis B: a novel diagnostic and prognostic indicator.BMC gastroenterology · 2025Article
- CRNDE, a Potential Therapeutic Target in Human Diseases.Current pharmaceutical design · 2025Review
- Long Non-coding RNAs as Key Modulators in Hypoxic-Ischemic Brain Injury: Implications for Neuroprotection.Current pharmaceutical design · 2025Review
- m6A methylation: a new frontier in epilepsy research and therapeutics.EXCLI journal · 2025Review
- Overexpression of long noncoding RNA colorectal neoplasia differentially expressed protects spinal cords against ischemia by targeting microRNA-181a-5p/Sirtuin-1 axis.Frontiers in neurologyArticle
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7 authors.
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Abstract
backgroundIschemia/reperfusion (I/R) injury is a severe brain disorder with currently limited effective treatments. This study aims to explore the role of N6-methyladenosine (m6A) modification and associated regulatory factors in I/R to identify potential therapeutic targets.
methodsWe utilized a middle cerebral artery occlusion (MCAO) rat model and SH-SY5Y cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to assess m6A levels and investigate the impact of METTL3 overexpression on long non-coding RNA (lncRNA) CRNDE expression. The effects of silencing lncRNA CRNDE on the interaction between YTHDC1 and ATG10 mRNA, as well as the stability of ATG10 mRNA, were evaluated. Additionally, apoptosis rates, pro-inflammatory and anti-inflammatory factor levels, ATG10 expression, and autophagic activity were analyzed to determine the effects of METTL3. The reverse effects of YTHDC1 overexpression were also examined.
resultsMCAO rats and OGD/R-treated SH-SY5Y cells exhibited reduced m6A levels. METTL3 overexpression significantly inhibited lncRNA CRNDE expression. Silencing lncRNA CRNDE mitigated OGD/R-induced apoptosis and inflammation in SH-SY5Y cells, while enhancing autophagy and stabilizing ATG10 mRNA. METTL3 overexpression decreased cell apoptosis, reduced the levels of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and increased IL-10 secretion. Furthermore, METTL3 overexpression upregulated ATG10 expression and promoted autophagy. Conversely, lncRNA CRNDE overexpression negated these effects.
conclusionThe inhibition of lncRNA CRNDE affects the interaction between YTHDC1 and ATG10 mRNA and stabilizes ATG10 mRNA, mediated by METTL3 overexpression. These findings suggest that targeting lncRNA CRNDE to reduce apoptosis, inhibit inflammation, increase ATG10 expression, and enhance autophagy could offer new therapeutic strategies for I/R injury.
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