 The study demonstrates that ANGP-TL4 is required for maintaining endothelial cell, EC, metabolic function, which is vital for vascular permeability and angiogenesis. Knockdown of ANGP-TL4 in ECs promotes lipace-mediated lipoprotein lipolysis, leading to increased FA uptake and oxidation, and decreased glucose utilization for angiogenic activation of ECs. The study also shows that mice with endothelial-specific deletion of ANGP-TL4 have decreased pathological neovascularization with stable vessel structures characterized by increased parasite coverage and reduced permeability. This article was authored by Balkrishna Shob, Catherine M. Citrin, Manas Sri, and others.