Wnt signaling in bone and muscle
Open accessAbstract
Wnt signaling plays key roles in many aspects of development. In this review, we will briefly describe the components of signaling pathways induced by Wnt ligands and then describe the current state of research as this applies to aspects of development and disease as it relates to skeletal muscle and bone. We will conclude with a discussion of the parallels and differences in Wnt signaling in these two contexts and how these pathways are being (or could potentially be) targeted for therapeutic treatment of musculoskeletal diseases. This article is part of a Special Issue entitled "Muscle Bone Interactions".
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Dickkopfs are secreted proteins capable of antagonizing Wnt signaling by inhibiting the coreceptors LRP5 and LRP6.
“Nevertheless, given that Dickkopfs are secreted proteins capable of antagonizing Wnt signaling by inhibiting the coreceptors LRP5 and LRP6 (43, 44), these findings suggest that increased Wnt signaling may also be involved in the increase in bone mass induced by ACVR2B/Fc.”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [44]
In “Wnt-Induced Signaling Pathways” (page unavailable), the paper says Dickkopf-family proteins inhibit canonical Wnt signaling by preventing Wnt ligands from binding LRP5/6. Our copy does not explicitly say that Dickkopfs are secreted; its statements about secretion concern Wnts and secreted frizzled-related proteins. (LLM, conf=0.82)
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A truncated Wnt7a retains full biological activity in skeletal muscle
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- [106]Bentzinger CF von Maltzahn J Dumont NA Stark DA Wang YX Nhan K Frenette J Cornelison DD Rudnicki MA Wnt7a stimulates myogenic stem cell motility and engraftment resulting in improved muscle strength J Cell Biol 2014 205 97 111 24711502 PMC3987134
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“Nevertheless, given that Dickkopfs are secreted proteins capable of antagonizing Wnt signaling by inhibiting the coreceptors LRP5 and LRP6 (43, 44), these findings suggest that increased Wnt signaling may also be involved in the increase in bone mass induced by ACVR2B/Fc.”
- Authors
- Rudnicki, M. A., & Williams, B. O.
- Affiliations
- University of Ottawa (CA)
- Van Andel Institute (US)
- Corresponding author
- Rudnicki, Michael A.
- Williams, Bart O.
- Venue
- Bone
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 80
- Pages
- 60-66
- ISSN
- 1873-2763 (ISSN-L)
- 8756-3282
- PMC
- PMC4600531
- OpenAlex
- W2139753760
- Cited by
- 132
- References
- 108
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 10 · 2023: 15 · 2022: 5 · 2021: 7 · 2020: 19 · 2019: 17 · 2018: 18 · 2017: 14 · 2016: 14
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Bone (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes for Health Research (MOP 81288 and MOP 12080)
- Muscular Dystrophy Association (ERA-132935)
- National Institutes of Health (R01AR44031)
- Canadian Stem Cell Network (RE05-084)
- Ontario Ministry of Research and Innovation
- Canada Research Chair Program
- Van Andel Research Institute
- NIH/NIAMS (R01 AR053293)
- Genentech
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- Wnt signaling, skeletal development, skeletal muscle development, musculoskeletal disorders, muscle-bone interaction, Wnt ligands
- MeSH terms
- Animals, Bone and Bones, Humans, Osteoblasts, Muscle, Skeletal, Wnt Proteins, Wnt Signaling Pathway
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