{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Todorov-Volgyi K"],"funding":["European Research Council"],"pagination":["325-336"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12880920"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(2)"],"pubmed_abstract":["Cerebral small vessel disease (SVD) is a common chronic cerebrovascular disorder with poorly understood pathomechanisms. Genetic studies have identified FOXF2 as a major risk gene for both SVD and stroke. FOXF2 encodes a transcription factor primarily expressed in brain pericytes and endothelial cells (ECs); however, its mechanistic role in cerebrovascular disease remains unknown. Here we show that Foxf2 maintains EC function through Tie2 signaling. RNA and chromatin sequencing identified FOXF2 as a transcriptional activator of Tie2 and other endothelial lineage-specific genes. The deletion of EC-specific Foxf2 in adult mice resulted in blood-brain barrier leakage, which worsened after experimental stroke. Proteomic analyses of Foxf2-deficient mouse brain-derived and human-induced pluripot"],"journal":["Nature neuroscience"],"pubmed_title":["The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling."],"pmcid":["PMC12880920"],"funding_grant_id":["865323"],"pubmed_authors":["Todorov MI","Gonzalez-Gallego J","Cernilogar FM","Cao J","Paquet D","Seker FB","Reyahi A","Schifferer M","Llovera G","Frerich S","Schillinger U","Malik R","Schroger L","Erturk A","Todorov-Volgyi K","Dichgans M","Plesnila N","Lichtenthaler SF","Carlsson P","Simons M","Muller SA","Roth S","Liesz A","Crusius D","Pedro LD","Schotta G"],"additional_accession":[]},"is_claimable":false,"name":"The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling.","description":"Cerebral small vessel disease (SVD) is a common chronic cerebrovascular disorder with poorly understood pathomechanisms. Genetic studies have identified FOXF2 as a major risk gene for both SVD and stroke. FOXF2 encodes a transcription factor primarily expressed in brain pericytes and endothelial cells (ECs); however, its mechanistic role in cerebrovascular disease remains unknown. Here we show that Foxf2 maintains EC function through Tie2 signaling. RNA and chromatin sequencing identified FOXF2 as a transcriptional activator of Tie2 and other endothelial lineage-specific genes. The deletion of EC-specific Foxf2 in adult mice resulted in blood-brain barrier leakage, which worsened after experimental stroke. Proteomic analyses of Foxf2-deficient mouse brain-derived and human-induced pluripot","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-15T06:32:12.899Z","creation":"2026-06-30T03:21:33.599Z"},"accession":"S-EPMC12880920","cross_references":{"pubmed":["41398477"],"doi":["10.1038/s41593-025-02136-5"]}}