Abstract: Glioma is a primary intracranial malignant tumor originating from neuroglial cells. Its pathogenesis involves the combined effects of multigene mutations and epigenetic abnormalities, which act through dysregulated angiogenesis, aberrant epigenetic regulation, imbalance between cell proliferation and apoptosis, immune escape, and other disrupted pathways. Glioma is characterized by high invasiveness, marked heterogeneity and pronounced vascularization. Prominent angiogenesis is one of its typical features. Classic angiogenic patterns in glioma include sprouting angiogenesis, vasculogenic mimicry, vessel co-option and intussusceptive angiogenesis, which give rise to abnormal vascular architectures. These abnormal vascular structures not only exacerbate glioma invasiveness but also increase therapeutic difficulty. Current outcomes with surgery, radiotherapy, and chemotherapy remain unsatisfactory. Anti-angiogenic therapy can alleviate edema, yet offers limited improvement in overall survival, while immune checkpoint inhibitor-based regimens are still in clinical trials. The four angiogenic mechanisms do not occur in isolation. They intersect and integrate across different stages of glioma development and exert distinct influences during progression across different glioma grades. Investigations into angiogenic factors and the mechanisms underlying dysregulated angiogenesis in glioma, immune escape and the imbalance between cell proliferation and apoptosis, represent frontier directions in research on glioma angiogenesis and therapeutic strategies.