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