Vascular calcification: lessons from scientific models

J Ren Care. 2009 Mar:35 Suppl 1:51-6. doi: 10.1111/j.1755-6686.2009.00065.x.

Abstract

Patients with chronic kidney disease have increased cardiovascular mortality from a combination of increased atherosclerotic disease, left ventricular hypertrophy and increased prevalence of vascular calcification (VC). Previously VC was thought to be a passive process which involved the deposition of calcium and phosphate into the vessel wall. However, recent studies have shown that VC is a highly regulated, cell-mediated process similar to bone formation, in that it is associated with expression of bone-related proteins, such as type I collagen and alkaline phosphatase. Animal and in vitro models of VC have shown that a multitude of factors including phosphate, matrix gla protein (MGP) and fetuin are involved in regulating VC. Certain factors induce calcification whereas others inhibit the process. Despite these insights, it is still not fully known how VC is regulated and a treatment for VC remains elusive. Ongoing research will hopefully elucidate these mechanisms and thereby produce targets for future therapeutic intervention. This review will highlight some of the scientific models of VC and how they have increased the understanding of this complex process.

Publication types

  • Review

MeSH terms

  • Alkaline Phosphatase / physiology
  • Animals
  • Apoptosis / physiology
  • Atherosclerosis / etiology
  • Calcinosis / epidemiology
  • Calcinosis / etiology*
  • Calcinosis / pathology
  • Calcinosis / therapy
  • Calcium-Binding Proteins / physiology
  • Cardiovascular Diseases / etiology
  • Cardiovascular Diseases / mortality
  • Collagen Type I / physiology
  • Diphosphates
  • Disease Models, Animal*
  • Extracellular Matrix Proteins / physiology
  • Humans
  • Hypertrophy, Left Ventricular / etiology
  • Inflammation
  • Kidney Failure, Chronic / complications*
  • Matrix Gla Protein
  • Mice
  • Osteopontin / physiology
  • Phosphorus / physiology
  • Prevalence
  • Risk Factors
  • Vascular Diseases / epidemiology
  • Vascular Diseases / etiology*
  • Vascular Diseases / pathology
  • Vascular Diseases / therapy
  • Vitamin D / therapeutic use
  • Vitamins / therapeutic use
  • alpha-Fetoproteins / physiology

Substances

  • Calcium-Binding Proteins
  • Collagen Type I
  • Diphosphates
  • Extracellular Matrix Proteins
  • Vitamins
  • alpha-Fetoproteins
  • Osteopontin
  • Vitamin D
  • Phosphorus
  • Alkaline Phosphatase