Ortega Nathalie, Behonick Danielle J, Werb Zena
Department of Anatomy, HSW1321, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0452, USA.
Trends Cell Biol. 2004 Feb;14(2):86-93. doi: 10.1016/j.tcb.2003.12.003.
Endochondral ossification, the process by which most of the skeleton is formed, is a powerful system for studying various aspects of the biological response to degraded extracellular matrix (ECM). In addition, the dependence of endochondral ossification upon neovascularization and continuous ECM remodeling provides a good model for studying the role of the matrix metalloproteases (MMPs) not only as simple effectors of ECM degradation but also as regulators of active signal-inducers for the initiation of endochondral ossification. The daunting task of elucidating their specific role during endochondral ossification has been facilitated by the development of mice deficient for various members of this family. Here, we discuss the ECM and its remodeling as one level of molecular regulation for the process of endochondral ossification, with special attention to the MMPs.
软骨内成骨是大多数骨骼形成的过程，是研究生物对降解细胞外基质（ECM）反应各个方面的有力系统。此外，软骨内成骨对新血管形成和持续的ECM重塑的依赖性，为研究基质金属蛋白酶（MMPs）的作用提供了一个良好的模型，这些酶不仅是ECM降解的简单效应器，也是软骨内成骨起始的活性信号诱导剂的调节剂。该家族各个成员基因敲除小鼠的培育，有助于阐明它们在软骨内成骨过程中具体作用这一艰巨任务。在此，我们将讨论ECM及其重塑作为软骨内成骨过程分子调控的一个层面，并特别关注MMPs。
