<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>de Rooij LPMH</submitter><funding>University Hospitals</funding><funding>European Research Council</funding><funding>Fonds Wetenschappelijk Onderzoek</funding><funding>Fundamental Clinical Mandate</funding><funding>ERC Research Grant</funding><funding>Flemish Supercomputer Center</funding><funding>Methusalem funding</funding><funding>Stichting tegen Kanker</funding><funding>Flemish Government</funding><funding>Leuven University</funding><funding>Hercules Foundation</funding><pubmed_abstract>&lt;h4>Aims&lt;/h4>SARS-CoV-2 infection causes COVID-19, which in severe cases evokes life-threatening acute respiratory distress syndrome (ARDS). Transcriptome signatures and the functional relevance of non-vascular cell types (e.g. immune and epithelial cells) in COVID-19 are becoming increasingly evident. However, despite its known contribution to vascular inflammation, recruitment/invasion of immune cells, vascular leakage and perturbed hemostasis in the lungs of severe COVID-19 patients, an in-depth interrogation of the endothelial cell (EC) compartment in lethal COVID-19 is lacking. Moreover, progressive fibrotic lung disease represents one of the complications of COVID-19 pneumonia and ARDS. Analogous features between idiopathic pulmonary fibrosis (IPF) and COVID-19 suggest partial simila</pubmed_abstract><journal>Cardiovascular research</journal><pagination>cvac139</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9452154</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The pulmonary vasculature in lethal COVID-19 and idiopathic pulmonary fibrosis at single cell resolution.</pubmed_title><pmcid>PMC9452154</pmcid><funding_grant_id>713758</funding_grant_id><funding_grant_id>1833317N</funding_grant_id><funding_grant_id>771883</funding_grant_id><funding_grant_id>ERC743074</funding_grant_id><pubmed_authors>Thienpont B</pubmed_authors><pubmed_authors>Mazzone M</pubmed_authors><pubmed_authors>Truong ACK</pubmed_authors><pubmed_authors>Jacobs W</pubmed_authors><pubmed_authors>Borri M</pubmed_authors><pubmed_authors>Menter T</pubmed_authors><pubmed_authors>Carmeliet P</pubmed_authors><pubmed_authors>Subramanian A</pubmed_authors><pubmed_authors>Tzankov A</pubmed_authors><pubmed_authors>Van Raemdonck D</pubmed_authors><pubmed_authors>van Dorpe J</pubmed_authors><pubmed_authors>Boudewijns R</pubmed_authors><pubmed_authors>Vinckier S</pubmed_authors><pubmed_authors>Amersfoort J</pubmed_authors><pubmed_authors>Feys S</pubmed_authors><pubmed_authors>Verleden S</pubmed_authors><pubmed_authors>Liesenborghs L</pubmed_authors><pubmed_authors>Dewerchin M</pubmed_authors><pubmed_authors>Sokol L</pubmed_authors><pubmed_authors>Meta E</pubmed_authors><pubmed_authors>Wauters E</pubmed_authors><pubmed_authors>Wauters J</pubmed_authors><pubmed_authors>Stalder AK</pubmed_authors><pubmed_authors>Philips G</pubmed_authors><pubmed_authors>Dendooven A</pubmed_authors><pubmed_authors>Van Buyten T</pubmed_authors><pubmed_authors>de Rooij LPMH</pubmed_authors><pubmed_authors>Gunst J</pubmed_authors><pubmed_authors>Teuwen LA</pubmed_authors><pubmed_authors>Lammens M</pubmed_authors><pubmed_authors>Lambrechts D</pubmed_authors><pubmed_authors>Jansen S</pubmed_authors><pubmed_authors>Kuehnel M</pubmed_authors><pubmed_authors>Eelen G</pubmed_authors><pubmed_authors>Neyts J</pubmed_authors><pubmed_authors>Van Mol P</pubmed_authors><pubmed_authors>Wuyts W</pubmed_authors><pubmed_authors>Ceulemans LJ</pubmed_authors><pubmed_authors>Schoonjans L</pubmed_authors><pubmed_authors>Becker LM</pubmed_authors><pubmed_authors>Rohlenova K</pubmed_authors><pubmed_authors>Boeckx B</pubmed_authors><pubmed_authors>Geldhof V</pubmed_authors><pubmed_authors>Libbrecht S</pubmed_authors><pubmed_authors>Haslbauer JD</pubmed_authors><pubmed_authors>Dumas SJ</pubmed_authors><pubmed_authors>Weynand B</pubmed_authors><pubmed_authors>Jonigk D</pubmed_authors></additional><is_claimable>false</is_claimable><name>The pulmonary vasculature in lethal COVID-19 and idiopathic pulmonary fibrosis at single cell resolution.</name><description>&lt;h4>Aims&lt;/h4>SARS-CoV-2 infection causes COVID-19, which in severe cases evokes life-threatening acute respiratory distress syndrome (ARDS). Transcriptome signatures and the functional relevance of non-vascular cell types (e.g. immune and epithelial cells) in COVID-19 are becoming increasingly evident. However, despite its known contribution to vascular inflammation, recruitment/invasion of immune cells, vascular leakage and perturbed hemostasis in the lungs of severe COVID-19 patients, an in-depth interrogation of the endothelial cell (EC) compartment in lethal COVID-19 is lacking. Moreover, progressive fibrotic lung disease represents one of the complications of COVID-19 pneumonia and ARDS. Analogous features between idiopathic pulmonary fibrosis (IPF) and COVID-19 suggest partial simila</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2025-04-04T23:13:48.279Z</modification><creation>2025-04-04T23:13:48.279Z</creation></dates><accession>S-EPMC9452154</accession><cross_references><pubmed>35998078</pubmed><doi>10.1093/cvr/cvac139</doi></cross_references></HashMap>