ArticleLife science alliance2024
Inflammatory risk contributes to post-COVID endothelial dysfunction through anti-ACKR1 autoantibody.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- Investigating apoptosis in peripheral blood mononuclear cells among the elderly in the post-COVID-19 era.BMC immunology · 2025Article
- Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health.GeroScience · 2025Review
- Kaurenoic acid is a potent inhibitor of SARS-CoV-2 RNA synthesis, virion assembly, and releaseFrontiers in microbiology · 2025Article
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subclinical vascular impairment can be exacerbated in individuals who experience sustained inflammation after COVID-19 infection. Our study explores the prevalence and impact of autoantibodies on vascular dysfunction in healthy COVID-19 survivors, an area that remains inadequately investigated. Focusing on autoantibodies against the atypical chemokine receptor 1 (ACKR1), COVID-19 survivors demonstrated significantly elevated anti-ACKR1 autoantibodies, correlating with systemic cytokines, circulating damaged endothelial cells, and endothelial dysfunction. An independent cohort linked these autoantibodies to increased vascular disease outcomes during a median 6.7-yr follow-up. We analyzed a single-cell transcriptome atlas of endothelial cells from diverse mouse tissues, identifying enriched
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