ArticleJournal of cardiovascular translational research2020
Knockdown of Long Non-Coding RNA AFAP1-AS1 Promoted Viability and Suppressed Death of Cardiomyocytes in Response to I/R In Vitro and In Vivo.
Article in Journal of cardiovascular translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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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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.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Long Non-Coding Ribonucleic Acid Taurine Up-Regulated Gene 1 Accelerates Ventricular Septal Defect Formation in Children.Brazilian journal of cardiovascular surgery · 2026Article
- Non-coding RNAs in congenital heart disease and placental development: Bridging molecular mechanisms to clinical biomarkers and therapies.Non-coding RNA research · 2026Review
- Lipid overload-induced RTN3 activation leads to cardiac dysfunction by promoting lipid droplet biogenesis.Cell death and differentiation · 2024Article
- Advances in non-coding RNA in tendon injuries.Frontiers in genetics · 2024Review
- Long noncoding RNA Kcnq1ot1 prompts lipopolysaccharide-induced acute lung injury by microRNA-7a-5p/Rtn3 axis.European journal of medical research · 2022Article
- Sex-Specific Alterations in Cardiac DNA Methylation in Adult Mice by Perinatal Lead Exposure.International journal of environmental research and public health · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNA) plays a pivotal role in the development of myocardial infarction (MI). The aim of this study was to investigate the effects of lncRNA actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) on cell cycle, proliferation, and apoptosis. RT-qPCR was used to detect the expression levels of AFAP1-AS1, miR-512-3p, and reticulon 3 (RTN3) in rat model of I/R. The simulated MI environment was constructed. MTT assay and flow cytometry were used to detect changes in cardiomyocyte viability and cell cycle/apoptosis after MI by AFAP1-AS1 silencing or RTN3 silencing. The targeting relationship of miR-512-3p and AFAP1-AS1 and RTN3 in cardiomyocytes was verified by dual luciferase reporter assay. The expression levels of AFAP1-AS1 and RTN3 were significantly upregulated in a rat model of LAD ligation (or MI) ligation, while the expression level of miR-512-3p was significantly reduced. Overexpressed AFAP1-AS1 and RTN3 promoted cardiomyocyte apoptosis and inhibited cardiomyocyte proliferation. MiR-512-3p was a direct target of AFAP1-AS1, and RTN3 was a direct target of miR-512-3p. AFAP1-AS1 promoted the progression of MI by targeting miR-512-3p. AFAP1-AS1 promoted the progression of MI by modulating the miR-512-3p/RTN3 axis. AFAP1-AS1 may be a potential therapy target for MI. Graphical Abstract The role of AFAP1-AS1 in regulating MI injury in vivo. (A) Effect of AFAP1-AS1 in MI injury in vivo. (B) The mRNA level of RTN3 in MI injury in vivo. (C) The protein level of RTN3 in MI injury in vivo. (D) Effect of miR-512-3p in MI model group. (E) TUNEL assay. *P < 0.05, **P < 0.01 vs the sham group; #P < 0.05, ##P < 0.01 vs the MI group.
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Registered trials
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