Receptor activator of nuclear factor-κB ligand (RANKL) is a member of the tumour necrosis factor family important in bone
remodelling. Recent evidence suggest that calcification in the vessel wall is equivalent to mechanisms mediating bone formation. This
review highlights the role of RANKL in vascular arterial calcification. Here, the relationship between RANKL, osteoprotegerin (OPG)
and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is discussed. Furthermore, we focus on the regulatory mechanisms
mediating RANKL gene expression and transcription in cells of the vessel wall. A better understanding of RANKL-mediated signalling
may help develop more sophisticated cell-based therapies to inhibit calcification of the vessel wall.
Keywords: Receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin (OPG), tumour necrosis factor-related apoptosisinducing
ligand (TRAIL), arterial calcification.
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