VEGF-A promotes both hemangiogenesis and lymphangiogenesis in inflammatory neovascularization by recruiting macrophages. This study used a novel model of inflammatory corneal neovascularization to investigate the role of VEGF-A in lymphangiogenesis. VEGF-A binds to VEGFR1 and VEGFR2 and is essential for hemangiogenesis. However, it also recruits macrophages, which release VEGF-C and VEGF-D, promoting lymphangiogenesis. Administration of VEGF Trap, a receptor-based fusion protein that neutralizes VEGF-A but not VEGF-C or -D, completely inhibited both hemangiogenesis and lymphangiogenesis. Similarly, mice transgenic for VEGF-A isoforms 164 or 188 showed reduced lymphangiogenesis and hemangiogenesis. Systemic depletion of bone marrow-derived cells or local depletion of macrophages also inhibited both processes. These findings suggest that VEGF-A recruits macrophages, which supply signals essential for both hemangiogenesis and lymphangiogenesis. Macrophages in inflamed corneas express VEGF-C and -D, further supporting their role in lymphangiogenesis. The study concludes that VEGF-A-mediated recruitment of macrophages is crucial for inflammatory neovascularization.VEGF-A promotes both hemangiogenesis and lymphangiogenesis in inflammatory neovascularization by recruiting macrophages. This study used a novel model of inflammatory corneal neovascularization to investigate the role of VEGF-A in lymphangiogenesis. VEGF-A binds to VEGFR1 and VEGFR2 and is essential for hemangiogenesis. However, it also recruits macrophages, which release VEGF-C and VEGF-D, promoting lymphangiogenesis. Administration of VEGF Trap, a receptor-based fusion protein that neutralizes VEGF-A but not VEGF-C or -D, completely inhibited both hemangiogenesis and lymphangiogenesis. Similarly, mice transgenic for VEGF-A isoforms 164 or 188 showed reduced lymphangiogenesis and hemangiogenesis. Systemic depletion of bone marrow-derived cells or local depletion of macrophages also inhibited both processes. These findings suggest that VEGF-A recruits macrophages, which supply signals essential for both hemangiogenesis and lymphangiogenesis. Macrophages in inflamed corneas express VEGF-C and -D, further supporting their role in lymphangiogenesis. The study concludes that VEGF-A-mediated recruitment of macrophages is crucial for inflammatory neovascularization.