ArticleActa pharmacologica Sinica2025
CircSARS-CV2-N1368 from SARS-CoV-2 impairs endothelial cell function through the upregulation of ATF7 to activate TLR4/NF-κB/ROS signaling.
Article in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Bridging neuroinflammation, oxidative stress, and neurogenesis: aromatic turmerone as a multifunctional modulator via NF-κB and Nrf2 pathways.Inflammopharmacology · 2026Review
- Rare pediatric multi-system thrombosis post-COVID-19: a three-year follow-up case report and narrative review on rivaroxaban for long-term management.Orphanet journal of rare diseases · 2026Review
- The regulatory mechanisms and translational applications of non-coding RNA in SARS-CoV-2 infection-related cardiovascular pathology.Frontiers in cardiovascular medicine · 2026Review
- Human cardiac organoids: multidimensional integration and clinical translation potential.Frontiers in pharmacology · 2026Review
- Functional Genomic Evidence for Candidate Small Viral RNA-Mediated Epigenetic Interference in SARS-CoV-1 and SARS-CoV-2.Computational and structural biotechnology journal · 2026Article
- Roles and Applications of Circular RNA in Virus Infection.International journal of molecular sciences · 2025Review
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Authors and funding
18 authors.
Funding
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Abstract
SARS-CoV-2 can encode circular RNAs (circRNAs); however, the potential effects of exogenous SARS-CoV-2 circRNAs on cardiovascular sequelae remain unknown. Three circRNAs derived from the nucleocapsid (N) gene of SARS-CoV-2, namely, circSARS-CV2-Ns, were identified for functional studies. In particular, circSARS-CV2-N1368 was shown to enhance platelet adhesiveness to endothelial cells (ECs) and inhibit EC-dependent vascular relaxation. Moreover, exogenous expression of circSARS-CV2-N1368 suppressed EC proliferation and migration and decreased angiogenesis and cardiac organoid beating. Mechanistically, we elucidated that circSARS-CV2-N1368 sponged the microRNA miR-103a-3p, which could reverse circSARS-CV2-N1368-induced EC damage. Additionally, activating transcription factor 7 (ATF7) was identified as a target gene of miR-103a-3p, and Toll-like receptor 4 (TLR4) was verified as a downstream gene of ATF7 that mediates circARS-CV2-N1368-induced activation of nuclear factor kappa B (NF-κB) signaling and ROS production in ECs. Importantly, the reactive oxygen species (ROS) scavenger NAC mitigated the circSARS-CV2-N1368-promoted EC impairment. Our findings reveal that the TLR4/NF-κB/ROS signal pathway is critical for mediating circSARS-CV2-N1368-promoted oxidative damage in ECs, providing insights into the endothelial impairment caused by circSARS-CV2-Ns.
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