Antiangiogenic VEGF ₁₆₅ b Regulates Macrophage Polarization via S100A8/S100A9 in Peripheral Artery Disease

Abstract

In our current study, we demonstrate that increased VEGF₁₆₅b expression in macrophages induces an antiangiogenic M1-like phenotype that directly impairs angiogenesis. VEGFR1 inhibition by VEGF₁₆₅b results in S100A8/S100A9-mediated calcium influx to induce an M1-like phenotype that impairs ischemic muscle revascularization and perfusion recovery.