GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327855/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327855GEOGSEfalseEndothelial FGF13 impairs angiogenesis by accelerating oxygen-independent HIF-1α degradation [RNA-Seq]Angiogenesis is a tightly regulated process essential for both development and disease, yet the role of fibroblast growth factor 13 (FGF13) in vascular remodeling has remained unclear. Here, we identify FGF13 as a key negative regulator of physiological and pathological angiogenesis. Using endothelial cell–specific knockout and overexpression mouse models, combined with retinal vascularization assays, hindlimb ischemia and myocardial infarction models, and in vitro endothelial cell functional assays, we demonstrate that loss of FGF13 enhances, whereas its overexpression impairs, neovascularization. Mechanistically, FGF13 binds to the PAS domain of HIF-1α and facilitates its interaction with RACK1, leading to oxygen-independent degradation of HIF-1α and suppression of downstream angiogenic signaling. Importantly, adenoviral overexpression of HIF-1α reversed the inhibitory effects of FGF13, confirming its essential role in mediating FGF13-driven angiogenic regulation. These findings reveal FGF13 as a critical endothelial-intrinsic brake on angiogenesis and suggest its potential as a therapeutic target in ischemic vascular disease.2026/04/18GSE327855GSM9667366GSM9667362GSM9667363GSM9667364GSM9667365GSM966736124676327855Homo sapiens