ArticleAmerican journal of translational research2019
Long non-coding RNA FOXD3-AS1 aggravates ischemia/reperfusion injury of cardiomyocytes through promoting autophagy.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review.Journal of cardiothoracic surgery · 2021Pooled it
- Silent controllers: non-coding RNAs drive autophagic response in myocardial ischemia reperfusion injury.Frontiers in cardiovascular medicine · 2026Review
- Comprehensive evaluation of non-coding RNA-mediated autophagy regulation in myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- Protective and deleterious effects of autophagy in the setting of myocardial ischemia/reperfusion injury: an overview.Molecular biology reports · 2022Review
- Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p.Iranian journal of public health · 2022Article
- lncRNA DHFRL1‑4 knockdown attenuates cerebral ischemia/reperfusion injury by upregulating the levels of angiogenesis‑related genes.International journal of molecular medicine · 2022Article
- Evaluating the Role of lncRNAs in the Incidence of Cardiovascular Diseases in Androgenetic Alopecia Patients.Cardiovascular toxicology · 2022Review
- Emerging Roles and Mechanisms of lncRNA FOXD3-AS1 in Human Diseases.Frontiers in oncology · 2022Review
- Epigenetic regulation in myocardial infarction: Non-coding RNAs and exosomal non-coding RNAs.Frontiers in cardiovascular medicine · 2022Review
- The Regulatory Role of Non-coding RNA in Autophagy in Myocardial Ischemia-Reperfusion Injury.Frontiers in pharmacology · 2022Review
- Selected In Situ Hybridization Methods: Principles and Application.Molecules (Basel, Switzerland) · 2021Review
- Involvement of non‑coding RNAs in the pathogenesis of myocardial ischemia/reperfusion injury (Review).International journal of molecular medicine · 2021Review
- Exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial I/R injury via p53-mediated autophagy and apoptosis.Molecular therapy. Nucleic acids · 2021Article
- Autophagy in cardiovascular diseases: role of noncoding RNAs.Molecular therapy. Nucleic acids · 2021Review
- Autophagy protects against cerebral ischemic reperfusion injury by inhibiting neuroinflammation.American journal of translational research · 2021Article
- Long Noncoding RNAs in Myocardial Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2021Review
- Long Non-coding RNA FER1L4 Mediates the Autophagy of Periodontal Ligament Stem Cells Under Orthodontic Compressive Force via AKT/FOXO3 Pathway.Frontiers in cell and developmental biology · 2021Article
- LncRNA PVT1 Knockdown Ameliorates Myocardial Ischemia Reperfusion Damage via Suppressing Gasdermin D-Mediated Pyroptosis in Cardiomyocytes.Frontiers in cardiovascular medicine · 2021Article
- LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2.Genes & genomics · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to investigate the role of long non-coding RNA (lncRNA) FOXD3 antisense RNA 1 (FOXD3-AS1) in myocardial Ischemia/reperfusion (I/R) injury. In our study, H9C2 cells were treated with oxygen-glucose deprivation and reoxygenation (OGD/R). RT-qPCR was performed to detect the expression level of lncRNA FOXD3-AS1 in OGD/R induced H9C2 cells. Then, pcDNA-lncRNA FOXD3-AS1 was transfected into H9C2 cells. The level of LC3 II was measured by immunofluorescence assay. And the expression of autophagy related genes were detected using western blot. In addition, 3-methyladenine (3 M), an autophagy inhibitor, was recruited to treat with H9C2 cells. The contents of creatine kinase (CK), CK isoenzymes (CK-MB), cardiac troponin I (cTnI), inflammation associated factors, reactive oxygen (ROS) and NO were evaluated by kits. Moreover, cell apoptosis was measured by a flow cytometry assay and the expression levels of apoptosis associated proteins were evaluated by western blot. Furthermore, the expression of NF-κB/iNOS/COX2 signaling were measured in our study. The results indicated that FOXD3-AS1 expression was increased in OGD/R-treated H9C2 cells and overexpression of FOXD3-AS1 upregulated the expression of LC3 II, Beclin1, ATG5 accompanied by a downregulated expression of p62. In addition, FOXD3-AS1 overexpression increased the levels of CK, CK-MB, cTnI, TNF-α, IL-1β, IL-6, ROS and NO, whereas the increase of above factors were reversed following treatment with 3 M. Moreover, FOXD3-AS1 overexpression enhanced the rate of apoptosis cells coupled with a decrease of Bcl-2 expression and an increase of Bax and cleaved caspase 3 expression, which were reversed by 3 M. Furthermore, FOXD3-AS1 overexpression promoted the activation of NF-κB/iNOS/COX2 signaling, which was blocked following treatment with 3 M. These findings demonstrate that overexpression of lncRNA FOXD3-AS1 aggravates myocardial I/R injury through promoting autophagy, which was regulated by activating NF-κB/iNOS/COX2 signaling.
Indexed as
Identifiers
31632535PMC6789269W2985408467What 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.