ArticleBioMed research international2020
CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia-Reperfusion Injury via Inhibiting miRNA-133 Expression.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 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
18 citing papers in PubMed.
- MicroRNA, MicroRNA-lncRNA and MicroRNA-Circular RNA axes, and exosomal MicroRNAs: driving exercise-induced cardioprotection in heart failure.Frontiers in cell and developmental biology · 2026Review
- Evidence and perspectives on miRNA, circRNA, and lncRNA in myocardial ischemia-reperfusion injury: a bibliometric study.Journal of cardiothoracic surgery · 2025Article
- MicroRNA-221 protects myocardial contractility in myocardial ischemia/reperfusion injury through phospholamban.PloS one · 2025Article
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Retracted: CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia-Reperfusion Injury via Inhibiting miRNA-133 Expression.BioMed research international · 2024Article
- Knockdown of Mmu-circ-0001380 Attenuates Myocardial Ischemia/Reperfusion Injury via Modulating miR-106b-5p/Phlpp2 Axis.Journal of cardiovascular translational research · 2023Article
- The Landscape of Circular RNAs in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Review
- LncRNA ROR modulates myocardial ischemia-reperfusion injury mediated by the miR-185-5p/CDK6 axis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway.Aging · 2022Article
- SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats.Annals of translational medicine · 2022Article
- Identification of a Novel Theranostic Signature of Metabolic and Immune-Inflammatory Dysregulation in Myocardial Infarction, and the Potential Therapeutic Properties of Ovatodiolide, a Diterpenoid Derivative.International journal of molecular sciences · 2022Article
- Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration.Frontiers in cardiovascular medicine · 2022Review
- An Overview of the Advances in Research on the Molecular Function and Specific Role of Circular RNA in Cardiovascular Diseases.BioMed research international · 2022Review
- Pretreatment with Panaxatriol Saponin Attenuates Mitochondrial Apoptosis and Oxidative Stress to Facilitate Treatment of Myocardial Ischemia-Reperfusion Injury via the Regulation of Keap1/Nrf2 Activity.Oxidative medicine and cellular longevity · 2022Article
- Involvement of non‑coding RNAs in the pathogenesis of myocardial ischemia/reperfusion injury (Review).International journal of molecular medicine · 2021Review
- Circular RNAs: Novel Players in the Oxidative Stress-Mediated Pathologies, Biomarkers, and Therapeutic Targets.Oxidative medicine and cellular longevity · 2021Review
- Saponins in Chinese Herbal Medicine Exerts Protection in Myocardial Ischemia-Reperfusion Injury: Possible Mechanism and Target Analysis.Frontiers in pharmacology · 2020Review
Corrections and comments
- Retraction · 2024-03-20Computer-Aided Content or Computer-Generated Content · Concerns/Issues about Data · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Results and/or Conclusions · Concerns/Issues about Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis project is aimed at investigating whether CircANXA2 can promote the apoptosis of myocardial cells by inhibiting miR-133 expression and thereby participate in the development of myocardial ischemia-reperfusion injury.
resultqRT-PCR results showed that compared with the control, the expression of CircANXA2 was upregulated and the expression level of miR-133 was significantly decreased in H/R-treated H9c2 cells. CircANXA2 overexpression increased LDH, MDA, SOD, and GSH-PX activity in H/R-treated H9c2 cells. At the same time, CircANXA2 overexpression inhibited the proliferation of H/R-treated cells, and CircANXA2 was able to induce cardiomyocyte apoptosis. Western blot results showed that after overexpression of CircANXA2, the proapoptotic genes Bax and cytochrome C was upregulated, while the antiapoptotic gene Bcl-2 was downregulated. In H9c2 cells, upregulating miR-133 can reverse the inhibition of proliferation induced by CircANXA2 overexpression and increase apoptosis.
conclusionsCircANXA2 promotes cardiomyocyte apoptosis in myocardial ischemia-reperfusion injury by inhibiting the expression of miR-133. CircANXA2 may be a potential target for myocardial ischemia-reperfusion injury.
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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.