The role of hedgehog signalling in skeletal health and disease
Abstract
Hedgehog ligands bind to protein patched homologue 1 (PTC), a conserved receptor that activates the GLI family of transcription factors, which are involved in development, disease and skeletal repair processes. During embryonic development, hedgehog signalling helps to pattern the limbs and plays a critical part in regulating chondrocyte differentiation and osteogenesis during the longitudinal growth of long bones. This signalling pathway also regulates mesenchymal cell differentiation during skeletal repair and regeneration. In pathologic and degenerative processes, such as osteoarthritis or cartilaginous tumour formation, hedgehog signalling is dysregulated. Several pharmacologic strategies can modulate hedgehog signalling, and targeting this pathway could lead to the development of novel therapeutic approaches. For example, by precisely regulating the level of activity of the hedgehog signalling pathway, the pace of degeneration in osteoarthritis could be slowed, bone repair could be enhanced, and cartilaginous tumour cell viability could be inhibited. As such, regulation of hedgehog signalling could be manipulated to safeguard skeletal health.
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Hedgehog signaling is important for maintaining bone homeostasis in adult mice, with down-regulation of hedgehog signaling being protective against bone loss.
“In addition to the roles that IHH and SHH play in regulating bone development, hedgehog signaling is also important for maintaining bone homeostasis in adult mice, with down-regulation of hedgehog signaling being protective against bone loss (41, 42).”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [42]
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Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight
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“In addition to the roles that IHH and SHH play in regulating bone development, hedgehog signaling is also important for maintaining bone homeostasis in adult mice, with down-regulation of hedgehog signaling being protective against bone loss (41, 42).”
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- Authors
- Alman, B. A.
- Affiliations
- Duke University (US)
- Corresponding author
- Alman, Benjamin A.
- ORCID
- Alman, Benjamin A.
- Venue
- Nature Reviews Rheumatology
- Published
- 2015-06-16
- Volume
- 11
- Issue
- 9
- Pages
- 552-560
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- OpenAlex
- W2205574727
- Cited by
- 141
- References
- 96
- Citations by year
- 2026: 8 · 2025: 12 · 2024: 15 · 2023: 12 · 2022: 17 · 2021: 17 · 2020: 18 · 2019: 12 · 2018: 7 · 2017: 11 · 2016: 10 · 2015: 2
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (01AR066765‑01)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Hedgehog Signaling Pathway Studies
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- Hedgehog signaling, skeletal health, osteoarthritis, bone regeneration, Gli transcription factors, chondrogenic differentiation, bone formation, limb development, mesenchymal differentiation, skeletal regeneration
- MeSH terms
- Animals, Bone and Bones, Bone Diseases, Humans, Signal Transduction, Hedgehog Proteins
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