ArticleAmerican journal of translational research2022
LncRNA FGD5-AS1 reduces cardiomyocyte apoptosis and inflammation by modulating Akt and miR-223-3p expression.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Long non-coding RNAs as molecular hubs integrating inflammatory and osteogenic pathways in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2026Review
- Identification of potential hub genes related to ferroptosis and hypoxia in dilated cardiomyopathy: a bioinformatic analysis with preliminary experimental validation.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Noncoding RNAs in myocardial ischemia/reperfusion injury and repair.Current opinion in physiology · 2025Article
- Mesenchymal Stem Cell Derived Exosomes Alleviates Hirschsprung-Associated Enterocolitis by Inhibiting AKT Phosphorylation in Macrophages Through miR-223.Stem cells international · 2025Article
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesLong non-coding RNAs (lncRNAs) are known to be involved in heart development and function. In this study, we aimed to explore the effect of the lncRNA FGD5 antisense RNA 1 (FGD5-AS1) on acute myocardial infarction (AMI) by targeting miR-223-3p.
methodsAn AMI model was established both in vivo and in vitro. The levels of FGD5-AS1, miR-223-3p and inflammatory factors were detected by real-time quantitative reverse transcription PCR. Cardiomyocyte apoptosis was assessed using TdT-mediated dUTP nick-end labeling assay. The protein levels of cleaved caspase-3, Bcl-2 and Bax were examined using Western blot. Cardiac function was evaluated using hemodynamic analysis and hematoxylin-eosin and Masson's trichrome staining. In addition, an underlying competitive endogenous RNA mechanism was revealed by bioinformatics analysis, dual-luciferase reporter assay and rescue experiments.
resultsWe found decreased expression of FGD5-AS1 in AMI. Furthermore, FGD5-AS1 expression significantly decreased the infarct size, improved cardiac performance and attenuated cardiac fibrosis by reducing myocardial apoptosis and inflammation. miR-223-3p was a direct target of FGD5-AS1. Moreover, miRNA-223-3p directly downregulated the expression of phosphorylated Akt in primary neonatal rat cardiomyocytes. Further experiments demonstrated that FGD5-AS1 modulated Akt activity to reduce myocardial injury through miR-223-3p.
conclusionThe FGD5-AS1/miR-223-3p/Akt pathway is involved in AMI, suggesting that FGD5-AS1 may act as a potential biomarker and therapeutic target for AMI.
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Identifiers
36247255PMC9556440W4306668988What OpenQuestion holds
Registered trials
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