{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pernomian L"],"funding":["NIA NIH HHS","NHLBI NIH HHS","NIAMS NIH HHS","NIH HHS","NIGMS NIH HHS"],"pagination":["1092-1113"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12530109"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["137(8)"],"pubmed_abstract":["<h4>Background</h4>Small artery remodeling and endothelial dysfunction are hallmarks of hypertension. Evidence supports a likely causal association between cardiovascular diseases and endothelial-to-mesenchymal transition (EndMT), a cellular transdifferentiation process in which endothelial cells (ECs) partially lose their identity and acquire mesenchymal phenotypes. EC reprogramming represents an innovative strategy in regenerative medicine to prevent deleterious effects induced by cardiovascular diseases.<h4>Methods</h4>Using partial reprogramming of ECs, via overexpression of Oct-3/4-Sox-2-Klf-4 (OSK) transcription factors, we aimed to bring ECs back to a youthful phenotype in hypertension. Primary ECs were infected with lentiviral vectors (LVs) containing the specific EC promoter Cdh5 "],"journal":["Circulation research"],"pubmed_title":["Single-Short Partial Reprogramming of the Endothelial Cells Decreases Blood Pressure via Attenuation of EndMT in Hypertensive Mice."],"pmcid":["PMC12530109"],"funding_grant_id":["R21 AG085331","S10 OD032271","P20 GM103499","R01 HL149762","R00 HL151889","R00 GM118885","R01 AR073172","R21 AR083066"],"pubmed_authors":["Nguyen V","Gleason K","Pernomian L","Biancardi VC","McCarthy CG","Aitken AV","Mohammed AD","Costa TJ","Wenceslau CF","Sinclair DA","Kubinak JL","Tan W","Fontes MT","Shazly T","Waigi EW","Wang Y"],"additional_accession":[]},"is_claimable":false,"name":"Single-Short Partial Reprogramming of the Endothelial Cells Decreases Blood Pressure via Attenuation of EndMT in Hypertensive Mice.","description":"<h4>Background</h4>Small artery remodeling and endothelial dysfunction are hallmarks of hypertension. Evidence supports a likely causal association between cardiovascular diseases and endothelial-to-mesenchymal transition (EndMT), a cellular transdifferentiation process in which endothelial cells (ECs) partially lose their identity and acquire mesenchymal phenotypes. EC reprogramming represents an innovative strategy in regenerative medicine to prevent deleterious effects induced by cardiovascular diseases.<h4>Methods</h4>Using partial reprogramming of ECs, via overexpression of Oct-3/4-Sox-2-Klf-4 (OSK) transcription factors, we aimed to bring ECs back to a youthful phenotype in hypertension. Primary ECs were infected with lentiviral vectors (LVs) containing the specific EC promoter Cdh5 ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-10T05:17:08.705Z","creation":"2026-06-10T03:07:59.488Z"},"accession":"S-EPMC12530109","cross_references":{"pubmed":["40899274"],"doi":["10.1161/CIRCRESAHA.124.324909","10.1161/circresaha.124.324909"]}}