Phosphate, oxidative stress, and nuclear factor-κB activation in vascular calcification

Kidney Int. 2011 May;79(10):1044-7. doi: 10.1038/ki.2010.548.

Abstract

Phosphate-induced vascular calcification, characterized by induction of osteogenic programs, mineral vesicle release, and apoptosis, is prevalent in patients with kidney disease. Zhao et al. provide a mechanistic link between phosphate-induced calcification and increased mitochondrial membrane potential, increased mitochondrial reactive oxygen species, activation of the nuclear factor-κB pathway, and subsequent expression of osteogenic genes and vascular mineralization. This link clarifies the intracellular mechanism of vascular calcification and may allow exploration of antioxidants as therapeutic agents for vascular calcification.

Publication types

  • Comment

MeSH terms

  • Antioxidants / therapeutic use
  • Calcinosis / etiology*
  • Calcinosis / metabolism
  • Glycerophosphates / pharmacology
  • Humans
  • NF-kappa B / metabolism*
  • Oxidative Stress*
  • Phosphates / metabolism
  • Phosphates / toxicity*
  • Reactive Oxygen Species / metabolism
  • Sodium-Phosphate Cotransporter Proteins / physiology
  • Vascular Diseases / etiology*
  • Vascular Diseases / metabolism

Substances

  • Antioxidants
  • Glycerophosphates
  • NF-kappa B
  • Phosphates
  • Reactive Oxygen Species
  • Sodium-Phosphate Cotransporter Proteins
  • beta-glycerophosphoric acid