{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["de Rooij LPMH"],"funding":["University Hospitals","European Research Council","Fonds Wetenschappelijk Onderzoek","Fundamental Clinical Mandate","ERC Research Grant","Flemish Supercomputer Center","Methusalem funding","Stichting tegen Kanker","Flemish Government","Leuven University","Hercules Foundation"],"pubmed_abstract":["<h4>Aims</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"],"journal":["Cardiovascular research"],"pagination":["cvac139"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9452154"],"repository":["biostudies-literature"],"pubmed_title":["The pulmonary vasculature in lethal COVID-19 and idiopathic pulmonary fibrosis at single cell resolution."],"pmcid":["PMC9452154"],"funding_grant_id":["713758","1833317N","771883","ERC743074"],"pubmed_authors":["Thienpont B","Mazzone M","Truong ACK","Jacobs W","Borri M","Menter T","Carmeliet P","Subramanian A","Tzankov A","Van Raemdonck D","van Dorpe J","Boudewijns R","Vinckier S","Amersfoort J","Feys S","Verleden S","Liesenborghs L","Dewerchin M","Sokol L","Meta E","Wauters E","Wauters J","Stalder AK","Philips G","Dendooven A","Van Buyten T","de Rooij LPMH","Gunst J","Teuwen LA","Lammens M","Lambrechts D","Jansen S","Kuehnel M","Eelen G","Neyts J","Van Mol P","Wuyts W","Ceulemans LJ","Schoonjans L","Becker LM","Rohlenova K","Boeckx B","Geldhof V","Libbrecht S","Haslbauer JD","Dumas SJ","Weynand B","Jonigk D"],"additional_accession":[]},"is_claimable":false,"name":"The pulmonary vasculature in lethal COVID-19 and idiopathic pulmonary fibrosis at single cell resolution.","description":"<h4>Aims</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","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2025-04-04T23:13:48.279Z","creation":"2025-04-04T23:13:48.279Z"},"accession":"S-EPMC9452154","cross_references":{"pubmed":["35998078"],"doi":["10.1093/cvr/cvac139"]}}