Sclerostin as a new key player in arteriovenous fistula calcification

Balci M., Kirkpantur A., Turkvatan A., Mandiroglu S., ÖZTÜRK E., Afsar B.

HERZ, vol.40, no.2, pp.289-297, 2015 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 40 Issue: 2
  • Publication Date: 2015
  • Doi Number: 10.1007/s00059-013-3992-y
  • Journal Name: HERZ
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.289-297
  • Süleyman Demirel University Affiliated: Yes

Abstract

The osteocyte-derived sclerostin has been shown to play a key inhibitor role in determining the normal extent of bone formation, and it consequently protects against the deleterious effects of uncontrolled bone growth. Sclerostin has been demonstrated to be upregulated during vascular smooth muscle cell calcification in vitro and has recently been identified in the human aorta at the protein level. Whether the effects of sclerostin on bone turnover and its vascular expression also translate into clinically significant changes in arteriovenous fistula patency is unknown.