Targeting Endothelial Dysfunction in Vascular Complications Associated with Diabetes
Figure 1
Under basal conditions, eNOS is kept in a “less active” state by binding to Cav-1. Activation of eNOS occurs by stimuli, (sheer stress, agonists such as acetylcholine, Ach), which causes an increase in intracellular Ca2+ and subsequent recruitment of cofactors and phosphorylation of the enzyme at S1177. Following which, eNOS is dissociated from Cav-1 and efficient EDNO production occurs. CaM: calmodulin; hsp90: heat shock protein 90.
