Oxidative Medicine and Cellular Longevity / 2018 / Article / Fig 9

Research Article

Parathyroid Hormone Causes Endothelial Dysfunction by Inducing Mitochondrial ROS and Specific Oxidative Signal Transduction Modifications

Figure 9

PTH-dependent endothelial dysfunction: hypothesis of molecular mechanisms involved. PTH, through IP3 production, induces increase of cytosolic calcium with relative increase in mitochondrial calcium uptake by MCU. The resultant mitochondrial calcium overload determines an increase of ROS production which in turn mediates the alteration of certain signaling (Bk, VEGFR) rather than other ones (Ach) by protein oxidation thus perturbing the endothelial functionality. Ru360 and MitoTEMPO, respectively, by inhibiting MCU and scavenging mitochondrial ROS, prevent perturbations in key signaling molecules for endothelial homeostasis.