Transcriptional control of chondrocyte fate and differentiation
Version of Record online: 26 SEP 2005
Copyright © 2005 Wiley-Liss, Inc.
Birth Defects Research Part C: Embryo Today: Reviews
Volume 75, Issue 3, pages 200–212, September 2005
How to Cite
Lefebvre, V. and Smits, P. (2005), Transcriptional control of chondrocyte fate and differentiation. Birth Defects Research Part C: Embryo Today: Reviews, 75: 200–212. doi: 10.1002/bdrc.20048
- Issue online: 26 SEP 2005
- Version of Record online: 26 SEP 2005
- National Institutes of Health. Grant Number: AR46249
- Arthritis Foundation
Chondrogenesis is an essential process in vertebrates. It leads to the formation of cartilage growth plates, which drive body growth and have primary roles in endochondral ossification. It also leads to the formation of permanent cartilaginous tissues that provide major structural support in the articular joints and respiratory and auditory tracts throughout life. Defects in chondrogenesis cause chondrodysostoses and chondrodysplasias. These skeletal malformation diseases account for a significant proportion of birth defects in humans and can dramatically affect a person's expectancy and quality of life. Chondrogenesis occurs when pluripotent mesenchymal cells commit to the chondrocyte lineage, and through a series of differentiation steps build and eventually remodel cartilage. This review summarizes and discusses our current knowledge and lack of knowledge about the chondrocyte differentiation pathway, from mesenchymal cells to growth plate and articular chondrocytes, with a main focus on how it is controlled by tissue patterning and cell differentiation transcription factors, such as, but not limited to, Pax1 and Pax9, Nkx3.1 and Nkx3.2, Sox9, Sox5 and Sox6, Runx2 and Runx3, and c-Maf. Birth Defects Research (Part C) 75:200–212, 2005. © 2005 Wiley-Liss, Inc.