ArticleCentral-European journal of immunology2021
Knockdown of circular RNA hsa_circ_0003204 inhibits oxidative stress and apoptosis through the miR-330-5p/Nod2 axis to ameliorate endothelial cell injury induced by low-density lipoprotein.
Article in Central-European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Knowledge Mapping of CircRNAs in AS Research from 2010 to 2025: Spotlight on Lipid Metabolism, Pyroptosis and Exosomes.Journal of inflammation research · 2026Article
- Dehydrodiisoeugenol targets NOD2 exerting dual effects against colitis and colorectal cancer: a double-edged sword.Molecular medicine (Cambridge, Mass.) · 2025Article
- Role of Circular RNAs in Atherosclerosis through Regulation of Inflammation, Cell Proliferation, Migration, and Apoptosis: Focus on Atherosclerotic Cerebrovascular Disease.Medicina (Kaunas, Lithuania) · 2023Review
- Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?Journal of clinical medicine · 2023Review
- Unfolding the genotype-to-phenotype black box of cardiovascular diseases through cross-scale modeling.iScience · 2022Article
- circ_0003204 regulates the osteogenic differentiation of human adipose-derived stem cells via miR-370-3p/HDAC4 axis.International journal of oral science · 2022Article
- MicroRNA-486-5p functions as a diagnostic marker for carotid artery stenosis and prevents endothelial dysfunction through inhibiting inflammation and oxidative stress.Bioengineered · 2022Article
- circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p.Computational and mathematical methods in medicine · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAtherosclerosis (AS) is the leading cause of cardiovascular disease. Circular RNA hsa_circ_0003204 (hsa_circ_0003204) was elevated in oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells. However, the role and molecular mechanism of hsa_circ_0003204 in the AS process have not been studied. MATERIAL AND
methodsHuman primary aortic endothelial cells (HAECs) were treated with low-density lipoprotein (ox-LDL) to establish the AS model. The viability of ox-LDL-induced HAECs was assessed by counting kit-8 (CCK8) assay. Reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) levels in ox-LDL-induced HAECs supernatant were evaluated with the relevant kits. The apoptosis of ox-LDL-induced HAECs was determined via flow cytometry assay. The expression of hsa_circ_0003204, miR-330-5p, and nucleotide-binding oligomerization domain 2 (Nod2) was analyzed through quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between hsa_circ_0003204 or Nod2 and miR-330-5p was verified by dual-luciferase reporter assay. Protein level of Nod2 was detected using western blot analysis.
resultsHsa_circ_0003204 and Nod2 were upregulated while miR-330-5p was decreased in ox-LDL-induced HAECs. Hsa_circ_0003204 depletion restrained the oxidative stress and apoptosis of ox-LDL-induced HAECs. Notably, hsa_circ_0003204 regulated Nod2 expression via sponging miR-330-5p in HAECs. Moreover, miR-330-5p inhibition restored the constraint of the oxidative stress and apoptosis of ox-LDL-induced HAECs caused by hsa_circ_0003204 silencing. Additionally, miR-330-5p targeted Nod2 and Nod2 enhancement abolished the repressive effects of miR-330-5p overexpression on the oxidative stress and apoptosis of ox-LDL-induced HAECs.
conclusionsHsa_circ_0003204 exhaustion mitigated endothelial cell injury through suppressing the oxidative stress and apoptosis in ox-LDL-induced HAECs via the miR-330-5p/Nod2 axis.
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