Regulation of bone mass by Wnt signaling.

By V. Krishnan, H. Bryant, O. MacDougald. Journal of Clinical Investigation, 2006

1,426 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0213f1d62861cedc62be46f20eb27994b7f2fc4c

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In Molecular Biology

1. Cristina Cruciat
2. R. Hen
3. Christof Niehrs
4. R. Jilka
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6. P. Ducy

Citations in the corpus

• Bone regeneration strategies: engineered scaffolds, bioactive molecules and stem cells Current stage and future perspectives (2018, neutral): “The strategies can be classified in three sub-categories: i) use of recombinant growth factors or a mixture of these growth factors that are associated with a natural matrix or calcium phosphate material carrier, ii) use of peptides, derived from extra-cellular matrix proteins, to target other cellu”
• Sclerostin Mediates Bone Response to Mechanical Unloading Through Antagonizing Wnt/β‐Catenin Signaling (2009, background): “Wnt/b-catenin signaling critically regulates bone mass.((8,9,38)) Recently, Wnt/b-catenin signaling was shown to be involved in the bone response to mechanical loading.”
• Function and biological roles of the Dickkopf family of Wnt modulators (2006, background): “…Wnt/b-catenin pathway plays a crucial role in bone formation and generally promotes an increase in bone mass by various mechanisms including renewal of stem cells, osteoblast proliferation, induction of osteoblastogenesis and inhibition of osteoblast and osteocyte apoptosis (Krishnan et al., 2006).”
• Secreted and transmembrane wnt inhibitors and activators. (2013, background): “Wnt/b-catenin signaling plays a central role in mammalian bone density regulation (Krishnan et al. 2006).”
• Molecular and cellular mechanisms of the anabolic effect of intermittent PTH. (2007, background): “Hence, intermittent PTH could increase osteoblast number via bursts of Wnt signaling, which would lead to increased differentiation and survival of osteoblasts and osteoblast progenitors [25,96].”
• Growth hormone, insulin-like growth factors, and the skeleton. (2008, background): “Indirectly, IGF-I may favor osteoblastogenesis by stabilizing -catenin, a signaling molecule used by the Wnt canonical signaling pathway, which is essential for osteoblastogenesis (147, 148).”
• Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum: an entero-bone endocrine axis (2008, background): “As a result, OPPG and high bone mass syndrome are viewed as Wnt-related diseases (Krishnan et al., 2006).”