ArticleJournal of cardiovascular pharmacology2021
CircRNA ACAP2 Is Overexpressed in Myocardial Infarction and Promotes the Maturation of miR-532 to Induce the Apoptosis of Cardiomyocyte.
Article in Journal of cardiovascular pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- DNA methylation and cardiovascular disease in humans: a systematic review and database of known CpG methylation sites.Clinical epigenetics · 2023Pooled it
- The emerging roles of small nucleolar RNAs, piwi-interacting RNAs, tRNA-derived small RNAs, and circular RNAs in the regulation of cardiac hypertrophy, ischemic heart disease, and heart failure.Genes & diseases · 2026Review
- Review
- Circular RNAs modulate cell death in cardiovascular diseases.Cell death discovery · 2025Review
- CircRNA Networks in CAD: Multi-Cellular Mechanisms and Clinical Potential.International journal of general medicine · 2025Review
- Identification of circular RNAs regulating cardiomyocyte proliferation in neonatal pig hearts.JCI insight · 2024Article
- Insights into circular RNAs: Biogenesis, function and their regulatory roles in cardiovascular disease.Journal of cellular and molecular medicine · 2023Review
- Promising roles of non-exosomal and exosomal non-coding RNAs in the regulatory mechanism and as diagnostic biomarkers in myocardial infarction.Journal of Zhejiang University. Science. B · 2023Review
- Circular RNAs: Biogenesis, Biological Functions, and Roles in Myocardial Infarction.International journal of molecular sciences · 2023Review
- Circular RNAs as a Diagnostic and Therapeutic Target in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Cell-Based and Selected Cell-Free Therapies for Myocardial Infarction: How Do They Compare to the Current Treatment Options?International journal of molecular sciences · 2022Review
- Extracellular Circular RNAs Act as Novel First Messengers Mediating Cell Cross-Talk in Ischemic Cardiac Injury and Myocardial Remodeling.Journal of cardiovascular translational research · 2022Review
- Emerging roles of circRNAs in the pathological process of myocardial infarction.Molecular therapy. Nucleic acids · 2021Review
- The Regulation Mechanisms and Clinical Application of MicroRNAs in Myocardial Infarction: A Review of the Recent 5 Years.Frontiers in cardiovascular medicine · 2021Review
- Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics.Frontiers in genetics · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractCircRNA ACAP2 and miR-532 both promotes the apoptosis of cardiomyocytes, which contributes to myocardial infarction (MI). Therefore, ACAP2 and miR-532 may interact with each other to participate in MI. Plasma samples from both patients with MI (n = 65) and healthy controls (n = 65) were subjected to RNA extractions and real-time quantitative polymerase chain reaction to analyze the expression of ACAP2, mature miR-532, and premature miR-532. Correlations among them were analyzed by Pearson's correlation coefficient. Expression of both mature miR-532 and premature miR-532 in cardiomyocytes with ACAP2 overexpression was analyzed by real-time quantitative polymerase chain reaction to study the effects of ACAP2 overexpression on the maturation of miR-532. The role of ACAP2 and miR-532 in regulating the apoptosis of cardiomyocytes induced by hypoxia was analyzed by cell apoptosis assay. In this study, we found that ACAP2 and mature miR-532 were both upregulated in plasma from patients with MI. ACAP2 and mature miR-532 were inversely correlated, whereas ACAP2 and premature miR-532 were not significantly correlated. In cardiomyocytes, overexpression of ACAP2 increased the expression of mature miR-532, but not premature miR-532. Cell apoptosis analysis showed that ACAP2 and miR-532 overexpression promoted the apoptosis of cardiomyocytes induced by hypoxia treatment. In addition, miR-532 inhibitor reduced the effects of ACAP2 overexpression. ACAP2 is overexpressed in MI and may promote the maturation of miR-532 to induce the apoptosis of cardiomyocyte.
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