Objective: To investigate the molecular mechanism by which hypoxia-induced glioma-derived exosomes regulate tumor angiogenesis through the JNK/HIF-1α pathway and its clinical implications. Methods: Hypoxic glioma models (1% O?) were established using U87MG and LN229 cells. Exosomes were isolated by ultracentrifugation and characterized by Transmission Electron Microscope (TEM), Nanoparticle Tracking Analysis (NTA), and Western blot. Transwell co-culture system was employed to analyze exosome effects on Human Umbilical Vein Endothelial Cells (HUVEC) tube formation and migration, with mechanistic validation using JNK inhibitor SP600125 and miR-210 inhibitor Targapremir-210. An orthotopic glioma model in nude mice was constructed for in vivo angiogenesis assessment via bioluminescence imaging and immunohistochemistry. Serum exosomal HIF-1α levels and survival data were analyzed in 60 glioma patients. Results: Hypoxia increased exosome secretion (P<0.05) with elevated HIF-1α, miR-210, miR-21 and miR-155 content. Exosomes activated the JNK/HIF-1α axis to upregulate VEGF expression in HUVECs (P<0.01), enhancing tube formation and migration. In vivo, exosome-treated tumors showed higher microvessel density (P<0.05). Clinically, serum exosomal HIF-1α correlated with tumor grade (r=0.68, P<0.001) and predicted poorer survival (14.4-month reduction, P=0.002). Conclusion: Hypoxic glioma exosomes drive angiogenesis via the JNK/HIF-1α/VEGF axis through delivering HIF-1α/miR-210, serving as both prognostic biomarker and therapeutic target.