TNFRSF11A and atherosclerosis: Since SOST is expressed in arterial tissues and antagonises the Wnt pathway involved in cardiovascular remodelling, inhibition of SOST can promote vascular calcification and the risk of cardiovascular events; thus, SOST produced in arterial tissue may provide a natural defence mechanism against atherosclerosis.81, 82, 83, 84 There is growing evidence that the RANKL/RANK/OPG system contributes to the formation of vascular calcification, and SOST can stimulate the secretion of RANKL.84, 85, 86 Importantly, past research suggests high circulating SOST may benefit the cardiovascular system.83