Novel aspects on RANK ligand and osteoprotegerin in osteoporosis and vascular disease

Calcif Tissue Int. 2004 Jan;74(1):103-6. doi: 10.1007/s00223-003-0011-y. Epub 2003 Oct 6.

Abstract

The clinical coincidence of osteoporosis and vascular disease has long indicated that common mediators may adversely affect bone metabolism and vascular integrity alike. Receptor activator of NF-kappaB ligand (RANKL) is an important cytokine for bone resorption that acts through its osteoclastic receptor, receptor activator of NF-kappaB (RANK), while osteoprotegerin serves as a decoy receptor that binds RANKL and prevents activation of RANK. Skeletal and vascular cells are sources and targets of RANKL and OPG both in vitro and in vivo. Modulation of the RANKL/RANK/OPG system in animals results in a skeletal and vascular phenotype, and administration of OPG may prevent osteoporosis and vascular calcification. Recent studies on OPG serum levels and gene polymorphisms also suggest an important role of this cytokine system in skeletal and vascular diseases. In summary, there is increasing evidence that RANKL and OPG may link the skeletal with the vascular system.

Publication types

  • Review

MeSH terms

  • Animals
  • Carrier Proteins / metabolism*
  • Glycoproteins / metabolism*
  • Humans
  • Membrane Glycoproteins / metabolism*
  • Models, Biological
  • Osteoporosis / drug therapy
  • Osteoporosis / metabolism*
  • Osteoprotegerin
  • RANK Ligand
  • Receptor Activator of Nuclear Factor-kappa B
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Receptors, Tumor Necrosis Factor
  • Vascular Diseases / drug therapy
  • Vascular Diseases / metabolism*

Substances

  • Carrier Proteins
  • Glycoproteins
  • Membrane Glycoproteins
  • Osteoprotegerin
  • RANK Ligand
  • Receptor Activator of Nuclear Factor-kappa B
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Tumor Necrosis Factor
  • TNFRSF11A protein, human
  • TNFRSF11B protein, human
  • TNFSF11 protein, human