2014
DOI: 10.14310/horm.2002.1552
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The sclerostin story: From human genetics to the development of novel anabolic treatment for osteoporosis

Abstract: Sclerosteosis and Van Buchem disease are two rare bone sclerosing disorders characterized by increased bone mineral density, tall stature and entrapment of cranial nerves due to overgrowth of a highly dense bone. Recent advances in human genetics have revealed the genetic background of these disorders by cloning the SOST gene, which is localized on chromosome region 17q12-q21 and codes for sclerostin. Sclerostin is a protein produced almost exclusively from osteocytes inhibiting bone formation by both osteobla… Show more

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Cited by 21 publications
(17 citation statements)
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“…Sclerostin is a protein encoded by the SOST gene and synthesized by osteocyte. It blocks the Wnt/β-catenin (an anti-anabolic bone effect), reducing bone formation [19]. Sclerostin may also induce adipogenesis in vitro through the same mechanism, i.e.…”
Section: Discussionmentioning
confidence: 99%
“…Sclerostin is a protein encoded by the SOST gene and synthesized by osteocyte. It blocks the Wnt/β-catenin (an anti-anabolic bone effect), reducing bone formation [19]. Sclerostin may also induce adipogenesis in vitro through the same mechanism, i.e.…”
Section: Discussionmentioning
confidence: 99%
“…Sclerostin is an inhibitor of the bone anabolic molecule wnt / beta-catenin (Yavropoulou et al, 2014). Mechanical stimulation of the skeletal system regulates sclerostin that allows bone forming osteoblasts to increase bone formation and overall bone density and strength (Moustafa et al, 2012).…”
Section: Physical Activity Bone Health and Molecular Pathways To Hementioning
confidence: 99%
“…All skeletal disturbances in mentioned disorders are associated with sclerostin, and can be explained by physiological functions of this compound. 5,11 Nowadays, it has become well-known that sclerostin belongs to Wnt inhibitors. Wnt/b-catenin signaling pathway is essential for normal physiological cell functions such as differentiation or proliferation.…”
Section: Anti-sclerostin Antibodiesmentioning
confidence: 99%
“…Data from previous studies concerning LRP4 protein mutations showed occurrence of aberrations of skeletal phenotypes in the form of increased bone mass. 5,[11][12][13] Genetic modifications of sclerostin activity were observed both during researches, and in naturally occurred diseases such as sclerosteosis and van Buchem's disease. It was precisely its inhibition, resulting in increased bone mineral density (BMD) that opened up the possibility of therapeutic use of the observed effects.…”
Section: Anti-sclerostin Antibodiesmentioning
confidence: 99%