ArticleCurrent issues in molecular biology2026
Endothelial Cell Activation by SARS-CoV-2 Spike Protein and Its RBD: Central Player of the Immunothrobotic Response in COVID-19.
Article in Current issues in molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- SARS-CoV-2 disrupts the integrity of a human blood-brain barrier model in the absence of infection.Journal of neurovirology · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
COVID-19 has been associated with an active immunothrombotic process. The involvement of endothelial cells (ECs) in the feedback loop of the inflammatory and thrombotic process characteristic of COVID-19, as well as its differences with other infectious inflammatory conditions, remains an area requiring further elucidation. This study aimed to assess the immunothrombotic phenotype induced by the SARS-CoV-2 Spike (S) protein and its receptor-binding domain (RBD) in endothelial-derived cell lines. HUVEC and EA.hy926 cell lines were exposed to S protein and to its RBD. Inflammatory, thrombotic, and fibrinolytic mediators were quantified. Molecular docking assays were conducted to identify potential EC receptors for S protein. EC activation was dependent on both protein concentration and stimulation time. An increased release of immunothrombotic biomarkers were observed in endothelial-derived cells exposed to the S protein and to its RBD. The RBD induced a stronger endothelial response. Molecular docking demonstrated high affinity and a possible interaction between the S protein and endothelial receptors: CD-141, CD-147, IL-6R, TLR 2, 4, and 7. These findings confirm that the S protein and its RBD can induce an immunothrombotic phenotype in EC-derived cell lines, potentially exacerbating the disease pathology. We propose possible endothelial receptors mediating this response.
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