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. Author manuscript; available in PMC: 2022 Apr 30.
Published in final edited form as: Circ Res. 2021 Apr 29;128(9):1344–1370. doi: 10.1161/CIRCRESAHA.121.318011

Figure 3. Role of NO and eNOS uncoupling in CAVD.

Figure 3.

NO signaling from VEC stimulates VIC quiescence through activation of GC/cGMP pathway and subsequent downregulation of RhoA pathway. It also prevents calcification through assisting with Notch1 translocation to the nucleus. eNOS uncoupling causes endothelial dysfunction, such that there is little to no NO signaling to VIC, increasing myofibroblastic activation and calcification. ROS is known to induce cell damage, Superoxide can further cause oxidative stress in VEC and VIC. Thick arrows are VIC-VEC signaling, thin are intracellular or autocrine VEC effects.