ArticleArchives of medical science : AMS2024
CircBAZ1B stimulates myocardial ischemia/reperfusion injury (MI/RI) by modulating miR-1252-5p/ATF3-mediated ferroptosis.
Article in Archives of medical science : AMS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- NEAT1 Coordinates a PDLIM5-CACNA1C Regulatory Program Associated with a Potentially Arrhythmogenic Cardiomyocyte State in the Border Zone During Early Myocardial Infarction.International journal of molecular sciences · 2026Article
- Sevoflurane Alleviates Myocardial Ischemia-Reperfusion Injury via the HMGB1/ACSL4 Pathway to Suppress Ferroptosis.Journal of biochemical and molecular toxicology · 2026Article
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
- Identification of key genes related to metabolic cell death in hepatic ischemia-reperfusion injury from transcriptome data and mechanism research using single-cell data.Frontiers in immunology · 2025Article
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Authors and funding
4 authors.
Funding
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Abstract
Introduction: Circular RNAs (circRNAs) have been implicated in myocardial ischemia (MI)/reperfusion injury (RI), yet their essential roles in MI/RI-induced ferroptosis have not been fully elucidated. Here, we focused on the biological function and regulatory mechanism of circBAZ1B, a circRNA derived from the bromodomain adjacent to the zinc finger domain 1B (BAZ1B) gene, in MI/RI progression. Material and methods: We used a rat model for MI/RI, assessing myocardial infarct size via electrocardiogram (ECG) and histological staining (hematoxylin and eosin [H&E] and 2,3,5-triphenyltetrazolium chloride [TTC]). Rat cardiomyoblasts (H9c2) were used for Results: The results showed that MI/RI was accompanied by ferroptosis. We also found that activating transcription factor 3 (ATF3) knockdown promoted myocardial cell viability and inhibited ferroptosis. Notably, activation of ATF3 transcription was demonstrated to upregulate the expression of its downstream target ACSL4. Functional analysis indicated that circBAZ1B promoted ATF3 expression via miR-1252-5p. Conclusions: The circBAZ1B/miR-1252-5p/ATF3 axis is crucial in MI/RI pathogenesis through ferroptosis regulation, offering a potential therapeutic target. Inhibiting this pathway may alleviate MI/RI effects, suggesting the need for further clinical studies.
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