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Sclerostin: Therapeutic Horizons Based Upon Its Actions.
MedLine Citation:
PMID:  22234741     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Inactivating mutations of the SOST gene cause a reduction in sclerostin levels and are associated with high bone mass. The clinical phenotypes, sclerosteosis and van Buchem's disease, were described in 1950s. Much later, it was learned that both diseases are due to loss-of-function mutations in the SOST gene. As a regulator of an important osteoanabolic pathway, Wnt, inactivation of SOST leads to a stimulation of the pathway it regulates. The high bone mass in patients with either sclerosteosis or van Buchem's disease is associated with unusual skeletal strength; they do not fracture. Knowledge of this molecule and its actions led rather quickly to the development of anti-sclerostin antibodies that lead to marked increases in bone mass in both animals and human subjects. Blocking sclerostin action with anti-sclerostin antibodies is a promising new therapeutic approach to osteoanabolic therapy of osteoporosis.
Authors:
Aline G Costa; John P Bilezikian
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-1-11
Journal Detail:
Title:  Current osteoporosis reports     Volume:  -     ISSN:  1544-2241     ISO Abbreviation:  -     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-1-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101176492     Medline TA:  Curr Osteoporos Rep     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Medicine, Division of Endocrinology, Metabolic Bone Diseases Unit, College of Physicians and Surgeons, Columbia University, 630 W. 168th St PH 8 West, Room864, New York, NY, 10032, USA.
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