Regulation and Function of Rankl in Arterial Calcification

Belinda   A. Di   Bartolo; Mary   M.   Kavurma

doi:10.2174/1381612820666140212205455

Abstract

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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DOI https://dx.doi.org/10.2174/1381612820666140212205455	Print ISSN 1381-6128
Publisher Name Bentham Science Publisher	Online ISSN 1873-4286

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Regulation and Function of Rankl in Arterial Calcification

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