ArticleMolecular medicine reports2020
lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- The nuclear receptor ROR-alpha is a putative novel myogenic regulator of the cardiomyocyte transcriptome, including the alpha-1A adrenergic receptor.American journal of physiology. Heart and circulatory physiology · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.Advanced healthcare materials · 2026Article
- Preliminary exploration of dynamic changes in circulating mitochondrial DNA (ΔmtDNA) as a prognostic biomarker for acute ST-segment elevation myocardial infarction patients: a prospective observational study.BMC cardiovascular disorders · 2026Observational
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2025Article
- Advances in Acute Myocardial Infarction (AMI) Diagnostics: Classical Biomarkers, Emerging Tools, and the Rise of Non-Invasive Sampling.Journal of cardiovascular translational research · 2025Review
- The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- RORA Regulates Autophagy in Hair Follicle Stem Cells by Upregulating the Expression Level of theBiomolecules · 2025Article
- DNMT1-driven methylation of RORA facilitates esophageal squamous cell carcinoma progression under hypoxia through SLC2A3.Journal of translational medicine · 2024Article
- Hereditary hemochromatosis with homozygous C282Y HFE mutation: possible clinical model to assess effects of elevated reactive oxygen species on the development of cardiovascular disease.Molecular and cellular biochemistry · 2024Review
- Screening of Biomarkers Related to Myocardial Infarction Based on the Construction of a ceRNA Regulation Network.Anatolian journal of cardiology · 2023Article
- Identification of Immuno-Inflammation-Related Biomarkers for Acute Myocardial Infarction Based on Bioinformatics.Journal of inflammation research · 2023Article
- A novel inflammation-associated prognostic signature for clear cell renal cell carcinoma.Oncology letters · 2022Article
- M6A-related lncRNAs predict clinical outcome and regulate the tumor immune microenvironment in hepatocellular carcinoma.BMC cancer · 2022Article
- Co-regulation of circadian clock genes and microRNAs in bone metabolism.Journal of Zhejiang University. Science. B · 2022Review
- RORA alleviates LPS-induced apoptosis of renal epithelial cells by promoting PGC-1α transcription.Clinical and experimental nephrology · 2022Article
- LncRNAs at the heart of development and disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2022Review
- Diagnostic significance of serum FGD5-AS1 and its predictive value for the development of cardiovascular diseases in patients with type 2 diabetes.Diabetology & metabolic syndrome · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FGD5 antisense RNA 1 (FGD5‑AS1) is a long non‑coding RNA in acute myocardial infarction (AMI), which is primarily caused by myocardial ischemia‑hypoxia. Retinoid acid receptor‑related orphan receptor α (RORA) is a key protector in maintaining heart function. However, the roles of FGD5‑AS1 and RORA in AMI have not previously been elucidated. The present study investigated the effect and mechanism of FGD5‑AS1 and RORA in human cardiomyocyte AC16 cells under hypoxia. Reverse transcription‑quantitative PCR and western blotting demonstrated that FGD5‑AS1 and RORA were downregulated in the serum of patients with AMI and hypoxia‑challenged AC16 cells. Functional experiments were performed via assays, flow cytometry and western blotting. In response to hypoxia, superoxide dismutase (SOD) activity was inhibited, but apoptosis rate and levels of reactive oxygen species and malondialdehyde were promoted in AC16 cells, accompanied by increased Bax and cleaved caspase‑3 expression levels, and decreased SOD2 and glutathione peroxidase 1 expression levels. However, hypoxia‑induced oxidative stress and apoptosis in AC16 cells were attenuated by ectopic expression of FGD5‑AS1 or RORA. Moreover, silencing RORA counteracted the suppressive role of FGD5‑AS1 overexpression in hypoxic injury. FGD5‑AS1 controlled RORA expression levels via microRNA‑195‑5p (miR‑195), as confirmed by dual‑luciferase reporter and RNA pull‑down assays. Consistently, miR‑195 knockdown suppressed hypoxia‑induced oxidative stress and apoptosis in AC16 cells, which was abrogated by downregulating FGD5‑AS1 or RORA. In conclusion, FGD5‑AS1 modulated hypoxic injury in human cardiomyocytes partially via the miR‑195/RORA axis, suggesting FGD5‑AS1 as a potential target in interfering with the progression of AMI.
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