ArticleFrontiers in immunology2026
SARS-CoV-2 spike S1-mediated HIF-2α activation in retinal endothelial cells suggests a mechanism contributing to post-COVID endothelial dysfunction.
Article in Frontiers in immunology, 2026. 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.
- Exercise and Cardiovascular Risk Modulation in Post-COVID Syndrome.Current atherosclerosis reports · 2026Review
- FNDC4 and FNDC5 Attenuate SARS-CoV-2 S1-Induced Inflammatory Responses in Human Adipose Tissue.European journal of clinical investigation · 2026Article
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Authors and funding
10 authors.
Funding
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Abstract
Background: Post-COVID-19 syndrome (PCS) is characterized by persistent symptoms such as fatigue, cardiovascular abnormalities, and cognitive impairment. Endothelial dysfunction (ED) has been proposed as a contributing factor, but underlying mechanisms remain unclear. We investigated whether SARS-CoV-2 spike protein subunit 1 (S1) is sufficient to induce ED in human retinal endothelial cells (HRECs) Methods: In this study, we characterized 41 PCS patients and 24 pre-pandemic healthy controls. The effects of recombinant S1 and plasma from patients with severe PCS on endothelial function were assessed in HRECs. Belzutifan was used as a pharmacologic probe to assess the role of HIF-2α signaling in S1- and plasma-associated endothelial responses. Results: PCS patients exhibited elevated erythropoietin, VEGF, and MCP-1 levels compared with controls. VEGF correlated with anti-S1 IgG and was upregulated at the mRNA level in S1-exposed HRECs. Additionally, Conclusion: These findings identify a spike-responsive, HIF-2α-associated ED pathway in retinal endothelial cells. Modulation of this pathway altered endothelial barrier responses to both recombinant S1 and plasma from patients with PCS, highlighting a candidate mechanism that may contribute to PCS-associated vascular dysfunction.
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