{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee ES"],"funding":["Human Frontier Science Program","NTU | Lee Kong Chian School of Medicine, Nanyang Technological University","Thomas and Stacey Siebel Foundation","National Healthcare Group","Additional Ventures","National Health Innovation Centre Singapore","Ministry of Education - Singapore"],"pagination":["e202402598"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11091471"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(7)"],"pubmed_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 "],"journal":["Life science alliance"],"pubmed_title":["Inflammatory risk contributes to post-COVID endothelial dysfunction through anti-ACKR1 autoantibody."],"pmcid":["PMC11091471"],"funding_grant_id":["RGY0069/2019","980072","Siebel Investigator","Strategic Academic Initiative","COVID19 CG008","T2EP30122-0008","ET1-2023-07"],"pubmed_authors":["Lye DC","Loh KM","Dalan R","Cheung C","Wee H","Ang LT","Tay KY","Renia L","Nguyen N","Law MC","Young BE","Fan BE","Lee ES","Lee IR","Goh LL","Chan MY","Lee KL","Chioh FW","Wazny V"],"additional_accession":[]},"is_claimable":false,"name":"Inflammatory risk contributes to post-COVID endothelial dysfunction through anti-ACKR1 autoantibody.","description":"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 ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-01T18:50:58.014Z","creation":"2026-05-19T03:07:10.036Z"},"accession":"S-EPMC11091471","cross_references":{"pubmed":["38740432"],"doi":["10.26508/lsa.202402598"]}}