Journal of Molecular Medicine

, Volume 86, Issue 4, pp 379–389

Mineral chaperones: a role for fetuin-A and osteopontin in the inhibition and regression of pathologic calcification

  • Willi Jahnen-Dechent
  • Cora Schäfer
  • Markus Ketteler
  • Marc D. McKee
Review

DOI: 10.1007/s00109-007-0294-y

Cite this article as:
Jahnen-Dechent, W., Schäfer, C., Ketteler, M. et al. J Mol Med (2008) 86: 379. doi:10.1007/s00109-007-0294-y

Abstract

Clinical nephrologists are well aware of the consequences of pathologic mineralization (calcification). Several studies have found a strong association between vascular and valvular mineralization and advanced or end-stage chronic kidney disease (CKD), with shorter survival times and increased morbidity. In the cardiology community, until quite recently, ectopic mineralization was considered harmless or even beneficial. Some still assume that atherosclerotic intima mineralization stabilizes atherosclerotic plaques, thus doing more good than harm. We suggest that vascular mineralization and indeed soft tissue mineralization in general may be a way in which the body deals with certain adverse situations involving local inflammation, associated tissue damage and tissue remodeling. Ectopic soft tissue mineralization resembles physiological bone mineralization in many ways. Markers of mineralizing bone also are present during soft tissue mineralization. We postulate that it may be possible to reverse soft tissue mineralization by applying selected principles of bone catabolism, namely mineral dissolution and phagocytosis. We consider putative strategies for therapeutic intervention to maximize the clearing of calcified debris particles. In particular, we discuss the roles of the plasma protein fetuin-A/alpha2HS-glycoprotein and the mineral-binding protein osteopontin in the prevention and possible regression of mineralization in disease.

Keywords

Fetuin-A Osteopontin Phagocytosis Macrophage Mineral Homeostasis CKD-MBD Vascular calcification Pathologic calcification Atherosclerosis 

Copyright information

© Springer-Verlag 2007

Authors and Affiliations

  • Willi Jahnen-Dechent
    • 1
  • Cora Schäfer
    • 1
  • Markus Ketteler
    • 2
  • Marc D. McKee
    • 3
  1. 1.Department of Biomedical Engineering, Biointerface LaboratoryRWTH Aachen University ClinicsAachenGermany
  2. 2.Medical Clinic IIIKlinikum Coburg gGmbHCoburgGermany
  3. 3.Faculty of Dentistry, and Department of Anatomy and Cell BiologyMcGill UniversityMontrealCanada

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