Minireview: In vivo analysis of Wnt signaling in bone

Donald A. Glass, Gerard Karsenty

Research output: Contribution to journalShort survey

162 Scopus citations

Abstract

Bone remodeling requires osteoblasts and osteoclasts working in concert to maintain a constant bone mass. The dysregulation of signaling pathways that affect osteoblast or osteoclast differentiation or function leads to either osteopenia or high bone mass. The discovery that activating and inactivating mutations in low-density lipoprotein receptor-related protein 5, a putative Wnt coreceptor, led to high bone mass and low bone mass in human beings, respectively, generated a tremendous amount of interest in the possible role of the Wnt signaling pathway in the regulation of bone remodeling. A number of mouse models have been generated to study a collection of Wnt signaling molecules that have been identified as regulators of bone mass. These mouse models help establish the canonical Wnt signaling pathway as a major regulator of chondrogenesis, osteoblastogenesis, and osteoclastogenesis. This review will summarize these advances.

Original languageEnglish (US)
Pages (from-to)2630-2634
Number of pages5
JournalEndocrinology
Volume148
Issue number6
DOIs
StatePublished - Jun 1 2007

ASJC Scopus subject areas

  • Endocrinology

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