Sun Margaret Man-Ger, Beier Frank
Department of Physiology and Pharmacology, Western University, and Children's Health Research Institute, London, Ontario, Canada.
Birth Defects Res C Embryo Today. 2014 Mar;102(1):74-82. doi: 10.1002/bdrc.21062.
Most of our bones form through the process of endochondral ossification, which is tightly regulated by the activity of the cartilage growth plate. Chondrocyte maturation through the various stages of growth plate physiology ultimately results in hypertrophy. Chondrocyte hypertrophy is an essential contributor to longitudinal bone growth, but recent data suggest that these cells also play fundamental roles in signaling to other skeletal cells, thus coordinating endochondral ossification. On the other hand, ectopic hypertrophy of articular chondrocytes has been implicated in the pathogenesis of osteoarthritis. Thus, a better understanding of the processes that control chondrocyte hypertrophy in the growth plate as well as in articular cartilage is required for improved management of both skeletal growth disorders and osteoarthritis. This review summarizes recent findings on the regulation of hypertrophic chondrocyte differentiation, the cellular mechanisms involved in hypertrophy, and the role of chondrocyte hypertrophy in skeletal physiology and pathophysiology.
我们大多数骨骼是通过软骨内成骨过程形成的,这一过程受到软骨生长板活动的严格调控。软骨细胞通过生长板生理的各个阶段成熟,最终导致肥大。软骨细胞肥大是纵向骨生长的重要促成因素,但最近的数据表明,这些细胞在向其他骨骼细胞发出信号方面也发挥着重要作用,从而协调软骨内成骨。另一方面,关节软骨细胞的异位肥大与骨关节炎的发病机制有关。因此,为了更好地管理骨骼生长障碍和骨关节炎,需要更深入地了解控制生长板以及关节软骨中软骨细胞肥大的过程。本综述总结了关于肥大软骨细胞分化调控、肥大相关细胞机制以及软骨细胞肥大在骨骼生理和病理生理中的作用的最新研究结果。