Duncan R L
Department of Orthopaedic Surgery, Physiology and Biophysics, Indiana University Medical Center, Indianapolis 46202, USA.
ASGSB Bull. 1995 Oct;8(2):49-62.
One physiologic consequence of extended periods of weightlessness is the rapid loss of bone mass associated with skeletal unloading. Conversely, mechanical loading has been shown to increase bone formation and stimulate osteoblastic function. The mechanisms underlying mechanotransduction, or how the osteoblast senses and converts biophysical stimuli into cellular responses has yet to be determined. For non-innervated mechanosensitive cells like the osteoblast, mechanotransduction can be divided into four distinct phases: 1) mechanocoupling, or the characteristics of the mechanical force applied to the osteoblast, 2) biochemical coupling, or the mechanism through which mechanical strain is transduced into a cellular biochemical signal, 3) transmission of signal from sensor to effector cell and 4) the effector cell response. This review examines the characteristics of the mechanical strain encountered by osteoblasts, possible biochemical coupling mechanisms, and how the osteoblast responds to mechanical strain. Differences in osteoblastic responses to mechanical strain are discussed in relation to the types of strain encountered and the possible transduction pathways involved.
长期失重的一个生理后果是与骨骼失载相关的骨量快速流失。相反，机械负荷已被证明可增加骨形成并刺激成骨细胞功能。机械转导的潜在机制，即成骨细胞如何感知并将生物物理刺激转化为细胞反应，尚未确定。对于像成骨细胞这样的无神经支配的机械敏感细胞，机械转导可分为四个不同阶段：1）机械耦合，即施加于成骨细胞的机械力的特性；2）生化耦合，即机械应变转化为细胞生化信号的机制；3）信号从传感器传递到效应细胞；4）效应细胞反应。本综述探讨了成骨细胞所遇到的机械应变的特性、可能的生化耦合机制，以及成骨细胞如何对机械应变作出反应。文中讨论了成骨细胞对机械应变反应的差异与所遇到的应变类型以及可能涉及的转导途径之间的关系。
