FLT1 and Hyperglycemia: Here we describe that SC mediate the impairment of neurite outgrowth caused by hyperglycaemia through increased secretion of vascular endothelial growth factor (VEGF) and altered fms-related tyrosine kinase 1 (FLT-1) receptor signaling, and that bevacizumab, a molecule that inhibits VEGF activity preventing the interaction to its receptors, in vitro prevented axonal outgrowth failure, and in vivo both rescued and restored in a dose-dependent fashion DN in rats.