Regulation and Function of Rankl in Arterial Calcification

Author(s): Belinda A. Di Bartolo, Mary M. Kavurma

Journal Name: Current Pharmaceutical Design

Volume 20 , Issue 37 , 2014

Become EABM
Become Reviewer

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 & PermissionsPrintExport Cite as

Article Details

VOLUME: 20
ISSUE: 37
Year: 2014
Published on: 22 September, 2014
Page: [5853 - 5861]
Pages: 9
DOI: 10.2174/1381612820666140212205455
Price: $65

Article Metrics

PDF: 25