Sclerostin as a new key player in arteriovenous fistula calcification

BALCI M. N., KIRKPANTUR A. A., TURKVATAN A., MANDIROGLU S., ÖZTÜRK E., AFSAR B.

HERZ, cilt.40, sa.2, ss.289-297, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 40 Sayı: 2
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1007/s00059-013-3992-y
  • Dergi Adı: HERZ
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.289-297
  • Hacettepe Üniversitesi Adresli: Evet

Özet

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.