Update on Wnt signaling in bone cell biology and bone disease

Research output: Contribution to journalArticle

258 Citations (Scopus)

Abstract

For more than a decade, Wnt signaling pathways have been the focus of intense research activity in bone biology laboratories because of their importance in skeletal development, bone mass maintenance, and therapeutic potential for regenerative medicine. It is evident that even subtle alterations in the intensity, amplitude, location, and duration of Wnt signaling pathways affects skeletal development, as well as bone remodeling, regeneration, and repair during a lifespan. Here we review recent advances and discrepancies in how Wnt/Lrp5 signaling regulates osteoblasts and osteocytes, introduce new players in Wnt signaling pathways that have important roles in bone development, discuss emerging areas such as the role of Wnt signaling in osteoclastogenesis, and summarize progress made in translating basic studies to clinical therapeutics and diagnostics centered around inhibiting Wnt pathway antagonists, such as sclerostin, Dkk1 and Sfrp1. Emphasis is placed on the plethora of genetic studies in mouse models and genome wide association studies that reveal the requirement for and crucial roles of Wnt pathway components during skeletal development and disease.

Original languageEnglish (US)
Pages (from-to)1-18
Number of pages18
JournalGene
Volume492
Issue number1
DOIs
StatePublished - Jan 15 2012

Fingerprint

Wnt Signaling Pathway
Bone Diseases
Cell Biology
Bone and Bones
Bone Development
Osteocytes
Bone Regeneration
Regenerative Medicine
Bone Remodeling
Genome-Wide Association Study
Osteoblasts
Osteogenesis
Maintenance
Therapeutics
Research

Keywords

  • β-catenin
  • Bone mineral density
  • Lrp5
  • Lrp6
  • Polymorphisms
  • R-spondin
  • Sclerostin

ASJC Scopus subject areas

  • Genetics

Cite this

Update on Wnt signaling in bone cell biology and bone disease. / Monroe, David G; McGee-Lawrence, Meghan E.; Oursler, Merry Jo; Westendorf, Jennifer J.

In: Gene, Vol. 492, No. 1, 15.01.2012, p. 1-18.

Research output: Contribution to journalArticle

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