TGFβ signaling in cartilage development and maintenance

• Published in: Birth defects research. Part C. Embryo today Vol. 102; no. 1; pp. 37 - 51
• Main Authors: Wang, Weiguang, Rigueur, Diana, Lyons, Karen M.
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.03.2014; Wiley Subscription Services, Inc
• Subjects: Animals; Biocompatibility; Biomedical materials; Birth defects; Cartilage; Cartilage (articular); Cartilage - growth & development; Cartilage diseases; Chondrogenesis - physiology; Congenital defects; Crosstalk; development; Genome-wide association studies; Genomes; Growth factors; Growth plate; Humans; Knee; maintenance; Mice; Modulators; Mutation; Osteoarthritis; Receptors; Signal Transduction; Signaling; TGFβ; Transducers; Transforming Growth Factor beta - metabolism; Transforming growth factor-b; TGFβ; development; signaling; maintenance; cartilage
• ISSN: 1542-975X; 1542-9768; 1542-9768
• DOI: 10.1002/bdrc.21058

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.