Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/120540
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Type: Journal article
Title: Regulation and function of RANKL in arterial calcification
Author: Di Bartolo, B.
Kavurma, M.
Citation: Current Pharmaceutical Design, 2014; 20(37):5853-5861
Publisher: Bentham Science
Issue Date: 2014
ISSN: 1381-6128
1873-4286
Statement of
Responsibility: 
Belinda A. Di Bartolo, Mary M. Kavurma
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
Rights: Copyright Status Unknown
RMID: 0030056049
DOI: 10.2174/1381612820666140212205455
Appears in Collections:Medicine publications

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