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Cited by 298

The DOI matches its Crossref record; 129 of the 129 references it cites were found in a registry or an index.

TGFβ signaling in cartilage development and maintenance

Open access
Wang, Weiguang, Rigueur, Diana, Lyons, Karen M.·2014·Birth Defects Research Part C: Embryo Today: Reviews

Abstract

Members of the transforming growth factor beta (TGFβ) superfamily of secreted factors play essential roles in nearly every aspect of cartilage formation and maintenance. However, the mechanisms by which TGFβs transduce their effects in cartilage in vivo remain poorly understood. Mutations in several TGFβ family members, their receptors, extracellular modulators, and intracellular transducers have been described, and these usually impact the development of the cartilaginous skeleton. Furthermore, genome‐wide association studies have linked components of the (TGFβ) superfamily to susceptibility to osteoarthritis. This review focuses on recent discoveries from genetic studies in the mouse regarding the regulation of TGFβ signaling in developing growth plate and articular cartilage, as well as the different modes of crosstalk between canonical and noncanonical TGFβ signaling. These new insights into TGFβ signaling in cartilage may open new prospects for therapies that maintain healthy articular cartilage. Birth Defects Research (Part C) 102:37–51, 2014. © 2014 Wiley Periodicals, Inc.

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Metadata

Authors
Wang, W., Rigueur, D., & Lyons, K. M.
Venue
Birth Defects Research Part C: Embryo Today: Reviews
Publisher
Wiley
Published
2014-03
Volume
102
Issue
1
Pages
37-51
ISSN
  • 1542-975X (ISSN-L)
  • 1542-9768
OpenAlex
W1603728190
Cited by
298
References
129
FWCI
8.70
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: TGFβ signaling in cartilage development and maintenance. https://app.cochat.ai/papers/10.1002/bdrc.21058
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Wang, W., Rigueur, D., & Lyons, K. M. (2014). TGFβ signaling in cartilage development and maintenance. Birth Defects Research Part C: Embryo Today: Reviews. https://doi.org/10.1002/bdrc.21058

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