The role of klotho on vascular calcification and endothelial function in chronic kidney disease

Semin Nephrol. 2014 Nov;34(6):578-85. doi: 10.1016/j.semnephrol.2014.09.003.

Abstract

Recent insights into novel roles of klotho in vascular biology make this primarily kidney-derived protein a possible candidate to form a link between chronic kidney disease and cardiovascular morbidity and mortality. Typical features of vascular dysfunction or structural abnormalities in the arterial wall are exacerbated in klotho-deficient states. Reported klotho functions include inhibition of local phosphate transport in vascular cells, phenotypic switches of vascular cellular elements into bone-forming cells, attenuation of matrix mineralization and calcification, and also preservation of endothelial functional properties and viability. To a large extent these insights rely on animal models of kidney or cardiovascular diseases. In this review the current state of knowledge on these issues is summarized, and we aim to provide a possible new perspective on cardiovascular disease in chronic kidney disease.

Keywords: CKD; Klotho; endothelial function; nitric oxide; phosphate; vascular calcification.

Publication types

  • Review

MeSH terms

  • Animals
  • Endothelium / physiopathology*
  • Fibroblast Growth Factor 3 / metabolism
  • Glucuronidase / deficiency
  • Glucuronidase / metabolism*
  • Humans
  • Klotho Proteins
  • Receptor, Fibroblast Growth Factor, Type 3 / metabolism
  • Renal Insufficiency, Chronic / metabolism*
  • Vascular Calcification / metabolism*

Substances

  • Fibroblast Growth Factor 3
  • Receptor, Fibroblast Growth Factor, Type 3
  • Glucuronidase
  • Klotho Proteins