Placental growth factor (PGF) is a pro-angiogenic growth factor that promotes vascular endothelial cell proliferation and migration through binding to FLT1/VEGFR-1 and neuropilin receptors 1. PGF isoform PlGF-2 binds neuropilin-1 and neuropilin-2 in a heparin-dependent manner, with expression patterns varying across cell types and disease contexts 2. Mechanistically, PGF drives angiogenesis via distinct pathways depending on cellular context. In diabetic retinopathy, PGF2α promotes retinal endothelial cell proliferation and tube formation through the PGF2α/PTGFR axis, activating Gq/CAMK2G/p38/ELK-1/FOS signaling to upregulate pro-angiogenic chemokines 3. Additionally, PGF2α induces inflammatory responses in retinal cells through FP receptor signaling 4. Clinically, PGF exhibits significant disease relevance. In bladder cancer, PGF functions as a key pro-angiogenic factor alongside VEGFA, with VEGFR1 being more highly expressed than VEGFR2 in tumor endothelial cells 1. Combined inhibition of PGF and VEGFA synergistically suppresses tumor growth and angiogenesis while enhancing CD8+ T cell infiltration, improving survival when combined with anti-PD-1 immunotherapy 1. In breast cancer, elevated PLGF-1 and neuropilin expression correlate with poor prognosis 2. These findings suggest PGF inhibition represents a novel therapeutic target for pathological angiogenesis-driven diseases.