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Since, podocytes adjacent to the glomerular endothelium also produce VEGF, the use of anti-VEGF therapy leads to proteinuria [214], and since VEGF not only controls EC proliferation in the setting of vessel formation but is also crucial for EC survival and the maintenance of vascular integrity, VEGF suppression impairs the regeneration ability of ECs by causing a deformed endothelial layer, leading to thrombosis [215]