ArticleScientific reports2025
Circ005699 regulates ox-LDL-induced vascular endothelial cell proliferation, autophagy and inflammation by sponging miR-636 and interacting with FTO.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- FTO-mediated GPX4 m6A modification in ferroptosis-induced DNA damage and inflammatory response during acute lung injury.Journal of bioenergetics and biomembranes · 2026Article
- SASP-driven vascular aging: unraveling the transcriptional nexus in endothelial senescence and cardiovascular disease.Histochemistry and cell biology · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Atherosclerosis (AS) is a chronic vascular disorder driven by endothelial dysfunction and inflammation, yet the roles of circular RNAs (circRNAs) in this process remain incompletely defined. Here, we identified circ0005699 as a significantly upregulated circRNA (fold change > 2, P < 0.05) in ox-LDL-treated macrophages and endothelial cells and confirmed its circular structure and stability by divergent PCR, RNase R resistance, and actinomycin D assays. qRT‒PCR analysis revealed elevated circ0005699 expression in serum from AS patients compared with that in serum from matched controls (n = 10 pairs, P < 0.01). Functional studies revealed that circ0005699 knockdown enhanced endothelial proliferation and tube formation, whereas overexpression suppressed angiogenesis. Mechanistically, circ0005699 acts as a sponge for miR-636, thereby upregulating solute carrier family 7 member 5 (SLC7A5) activity and activating mTORC1 signalling, which inhibits autophagy. In parallel, circ0005699 interacts with the RNA demethylase FTO through its N-terminus, stabilizing EGR1 mRNA by reducing m6A modification. Increased EGR1 expression promoted inflammatory responses (IL-6, IL-1β, and ICAM-1) while limiting endothelial proliferation, and these effects were abolished by EGR1 knockdown. Together, these findings define circ0005699 as a stable, upregulated circRNA that orchestrates AS progression through both the circ0005699/miR-636/SLC7A5-mTORC1/autophagy axis and the circ0005699/FTO-EGR1 inflammatory pathway, providing a potential biomarker and therapeutic target in AS.
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