<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nicolai L</submitter><funding>European Research Council</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>Deutsches Zentrum für Herz-Kreislaufforschung</funding><funding>Deutsche Herzstiftung</funding><pagination>2020-2031</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10174338</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(8)</volume><pubmed_abstract>Long COVID is a public health emergency affecting millions of people worldwide, characterized by heterogeneous symptoms across multiple organ systems. Here, we discuss the current evidence linking thromboinflammation to postacute sequelae of COVID-19. Studies have found persistence of vascular damage with increased circulating markers of endothelial dysfunction, coagulation abnormalities with heightened thrombin generation capacity, and abnormalities in platelet counts in postacute sequelae of COVID-19. Neutrophil phenotype resembles acute COVID-19 with an increase in activation and Neutrophil Extracellular Trap formation. These insights are potentially linked by elevated platelet-neutrophil aggregate formation. This hypercoagulable state in turn can lead to microvascular thrombosis, evide</pubmed_abstract><journal>Journal of thrombosis and haemostasis : JTH</journal><pubmed_title>Thromboinflammation in long COVID-the elusive key to postinfection sequelae?</pubmed_title><pmcid>PMC10174338</pmcid><funding_grant_id>512460086</funding_grant_id><funding_grant_id>B06</funding_grant_id><funding_grant_id>A07</funding_grant_id><funding_grant_id>413635475</funding_grant_id><funding_grant_id>SFB 1123</funding_grant_id><pubmed_authors>Stark K</pubmed_authors><pubmed_authors>Kaiser R</pubmed_authors><pubmed_authors>Nicolai L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Thromboinflammation in long COVID-the elusive key to postinfection sequelae?</name><description>Long COVID is a public health emergency affecting millions of people worldwide, characterized by heterogeneous symptoms across multiple organ systems. Here, we discuss the current evidence linking thromboinflammation to postacute sequelae of COVID-19. Studies have found persistence of vascular damage with increased circulating markers of endothelial dysfunction, coagulation abnormalities with heightened thrombin generation capacity, and abnormalities in platelet counts in postacute sequelae of COVID-19. Neutrophil phenotype resembles acute COVID-19 with an increase in activation and Neutrophil Extracellular Trap formation. These insights are potentially linked by elevated platelet-neutrophil aggregate formation. This hypercoagulable state in turn can lead to microvascular thrombosis, evide</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Aug</publication><modification>2025-04-19T03:47:23.463Z</modification><creation>2024-11-09T21:34:32.438Z</creation></dates><accession>S-EPMC10174338</accession><cross_references><pubmed>37178769</pubmed><doi>10.1016/j.jtha.2023.04.039</doi></cross_references></HashMap>