
The role of histone deacetylase 4 during chondrocyte hypertrophy and endochondral bone development
Author(s) -
Zhi Chen,
Zhiwei Zhang,
Li Guo,
Xiaochun Wei,
Yang Zhang,
Xiaojian Wang,
Lei Wei
Publication year - 2020
Publication title -
bone and joint research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.639
H-Index - 31
ISSN - 2046-3758
DOI - 10.1302/2046-3758.92.bjr-2019-0172.r1
Subject(s) - endochondral ossification , chondrocyte , hdac4 , trichostatin a , microbiology and biotechnology , histone deacetylase , muscle hypertrophy , chondrogenesis , cartilage , runx2 , ossification , bone growth , biology , endocrinology , cancer research , medicine , histone , anatomy , transcription factor , genetics , gene
Chondrocyte hypertrophy represents a crucial turning point during endochondral bone development. This process is tightly regulated by various factors, constituting a regulatory network that maintains normal bone development. Histone deacetylase 4 (HDAC4) is the most well-characterized member of the HDAC class IIa family and participates in different signalling networks during development in various tissues by promoting chromatin condensation and transcriptional repression. Studies have reported that HDAC4-null mice display premature ossification of developing bones due to ectopic and early-onset chondrocyte hypertrophy. Overexpression of HDAC4 in proliferating chondrocytes inhibits hypertrophy and ossification of developing bones, which suggests that HDAC4, as a negative regulator, is involved in the network regulating chondrocyte hypertrophy. Overall, HDAC4 plays a key role during bone development and disease. Thus, understanding the role of HDAC4 during chondrocyte hypertrophy and endochondral bone formation and its features regarding the structure, function, and regulation of this process will not only provide new insight into the mechanisms by which HDAC4 is involved in chondrocyte hypertrophy and endochondral bone development, but will also create a platform for developing a therapeutic strategy for related diseases. Cite this article: Bone Joint Res. 2020;9(2):82–89.