ArticleKorean circulation journal2026
PDE4D Mediates the Cardiac Ischemia Reperfusion Injury and Is m6A Modified by METTL14.
Article in Korean circulation journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Epitranscriptomic Regulation of Cardiac Ischemia-Reperfusion Injury: Unveiling the METTL14/IGF2BP1/PDE4D Axis.Korean circulation journal · 2026Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesCardiac ischemia-reperfusion (I/R) injury is a major contributor to morbidity following myocardial infarction. While PDE4D has been implicated in cerebral I/R injury, its role and regulatory mechanisms in the cardiac context remain unclear.
methodsPDE4D expression was analyzed using quantitative polymerase chain reaction and Western blot. Apoptosis was assessed by TUNEL staining, flow cytometry, and detection of caspase-3, Bax, and Bcl-2 levels. N6-methyladenosine (m6A) modification of PDE4D was examined via methylated RNA immunoprecipitation, luciferase reporter assays, and RNA stability measurements. The interaction between IGF2BP1 and PDE4D was confirmed by RNA immunoprecipitation.
resultsPDE4D was significantly upregulated in I/R-injured myocardium and in H9c2 cardiomyocytes subjected to hypoxia/reoxygenation. Knockdown of PDE4D reduced infarct size, suppressed apoptosis, and improved cell viability. METTL14 mediated m6A methylation at 2 conserved sites within PDE4D mRNA, thereby enhancing its RNA stability. Silencing METTL14 decreased PDE4D expression and reduced its transcript stability. IGF2BP1 recognized m6A-modified PDE4D and promoted its RNA stability; ablation of IGF2BP1 abolished the effects of METTL14. Overexpression of PDE4D reversed the cardioprotective effects resulting from METTL14 silencing.
conclusionsMETTL14 stabilizes PDE4D mRNA through m6A methylation, which is recognized by IGF2BP1, thereby exacerbating cardiac I/R injury.
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