Sost Deficiency does not Alter Bone’s Lacunar or Vascular Porosity in Mice

Sost Deficiency does not Alter Bone’s Lacunar or Vascular Porosity in Mice

SCLEROSTIN (Sost) is expressed predominantly in osteocytes acting as a negative regulator of bone formation. In humans, mutations in the SOST gene lead to skeletal overgrowth and increased bone mineral density, suggesting that SCLEROSTIN is a key regulator of bone mass. The function of SCLEROSTIN as...

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Bibliographic Details
Main Authors: Henry Mosey, Juan A. Núñez, Alice Goring, Claire E. Clarkin, Katherine A. Staines, Peter D. Lee, Andrew A. Pitsillides, Behzad Javaheri
Format: Article
Language:English
Published: Frontiers Media S.A. 2017-09-01
Series:Frontiers in Materials
Subjects:
Sost
osteocyte
vascular porosity
microCT
lacunar porosity
Online Access:http://journal.frontiersin.org/article/10.3389/fmats.2017.00027/full

Internet

http://journal.frontiersin.org/article/10.3389/fmats.2017.00027/full

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