Figure 2. Primary cilia activation by fluid shear stress and NO signaling in vascular endothelia.

The illustration above depicts the bending of primary cilia during fluid shear stress and the consequent biochemical production and release of nitric oxide (NO) which is dependent on the activation of endothelial primary cilia in the vasculature (Left panel). The bending of cilia by fluid-shear stress activates the mechanosensory polycystins complex and initiates biochemical synthesis and the release of NO. This biochemical cascade involves extracellular calcium influx (Ca²⁺), followed by the activation of various calcium-dependent proteins, including calmodulin (CaM), protein kinase C (PKC) and Akt/PKB (Right panel). Figure is adopted from [73].