Regulation and function of Rankl in arterial calcification

Belinda A. Di Bartolo, Mary M. Kavurma

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)5853-5861
Number of pages9
JournalCurrent Pharmaceutical Design
Volume20
Issue number37
Publication statusPublished or Issued - 1 Mar 2014
Externally publishedYes

Keywords

  • Arterial calcification
  • Osteoprotegerin (OPG)
  • Receptor activator of nuclear factor-κB ligand (RANKL)
  • Tumour necrosis factor-related apoptosisinducing ligand (TRAIL)

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery

Cite this