Poyatos Dorado, PaulaGratacòs-Aurich, MiquelAguilar, DanielLuque, NeusBonnin Vilaplana, MarcEizaguirre, SaioaCascante i Serratosa, MartaOrriols Martínez, RamonTura-Ceide, Olga2026-01-272026-01-272025-11-212589-0042https://hdl.handle.net/2445/226274Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused significant global morbidity since 2019. Long COVID, characterized by persistent symptoms after acute infection, may involve endothelial injury. We analyzed endothelial colony-forming cells (ECFCs) from post-COVID-19 patients at 3- and 6-month post-infection, comparing them with healthy controls and stratifying by prior pulmonary embolism (PE). Transcriptomic profiling identified differentially expressed genes (DEGs) associated with endothelial homeostasis, inflammation, oxidative stress, and thrombosis. Post-COVID ECFCs showed downregulation of NOS3, KLF2, ANGPT1, PIK3R3, GBX2, GDF6, SMAD6, SRC, and TGFB1, and upregulation of CASP1, CXCL5, IL12A, SOD2, TIMP3, and TLR2. Minimal differences were observed between 3 and 6-month samples. PE patients showed downregulation of thrombosis-related genes such as PTGS2 and ACKR3. These findings indicate sustained endothelial dysfunction and inflammation up to 6 months post-infection, highlighting the importance of long-term monitoring and potential therapeutic strategies to support vascular health in post-COVID-19 patients.120 p.application/pdfengcc-by (c) Poyatos, P. et al., 2025http://creativecommons.org/licenses/by/4.0/EndoteliEmbòlia pulmonarCOVID-19EndotheliumPulmonary embolismCOVID-19info:eu-repo/semantics/article7644322026-01-27info:eu-repo/semantics/openAccess