Proctor Carole J, Gartland Alison
MRC/Arthritis Research UK Centre for Musculoskeletal Ageing (CIMA), Newcastle University, Newcastle upon Tyne, UK; Musculoskeletal Research Group, Institute of Cellular Medicine, Medical School, Newcastle University, Newcastle upon Tyne, UK.
MRC/Arthritis Research UK Centre for Musculoskeletal Ageing (CIMA), Newcastle University, Newcastle upon Tyne, UK; Department of Oncology and Metabolism, University of Sheffield Medical School, Sheffield, UK.
Front Endocrinol (Lausanne). 2016 Jun 13;7:61. doi: 10.3389/fendo.2016.00061. eCollection 2016.
Bone remodeling is the continuous process of bone resorption by osteoclasts and bone formation by osteoblasts, in order to maintain homeostasis. The activity of osteoclasts and osteoblasts is regulated by a network of signaling pathways, including Wnt, parathyroid hormone (PTH), RANK ligand/osteoprotegrin, and TGF-β, in response to stimuli, such as mechanical loading. During aging there is a gradual loss of bone mass due to dysregulation of signaling pathways. This may be due to a decline in physical activity with age and/or changes in hormones and other signaling molecules. In particular, hormones, such as PTH, have a circadian rhythm, which may be disrupted in aging. Due to the complexity of the molecular and cellular networks involved in bone remodeling, several mathematical models have been proposed to aid understanding of the processes involved. However, to date, there are no models, which explicitly consider the effects of mechanical loading, the circadian rhythm of PTH, and the dynamics of signaling molecules on bone remodeling. Therefore, we have constructed a network model of the system using a modular approach, which will allow further modifications as required in future research. The model was used to simulate the effects of mechanical loading and also the effects of different interventions, such as continuous or intermittent administration of PTH. Our model predicts that the absence of regular mechanical loading and/or an impaired PTH circadian rhythm leads to a gradual decrease in bone mass over time, which can be restored by simulated interventions and that the effectiveness of some interventions may depend on their timing.
骨重塑是破骨细胞进行骨吸收和成骨细胞进行骨形成的持续过程,以维持体内平衡。破骨细胞和成骨细胞的活性受包括Wnt、甲状旁腺激素(PTH)、RANK配体/骨保护素和转化生长因子-β等信号通路网络的调节,以响应诸如机械负荷等刺激。在衰老过程中,由于信号通路失调,骨量会逐渐流失。这可能是由于随着年龄增长身体活动减少和/或激素及其他信号分子的变化。特别是,诸如PTH等激素具有昼夜节律,在衰老过程中可能会被打乱。由于骨重塑涉及的分子和细胞网络的复杂性,已经提出了几种数学模型来帮助理解其中涉及的过程。然而,迄今为止,尚无明确考虑机械负荷、PTH昼夜节律以及信号分子动力学对骨重塑影响的模型。因此,我们使用模块化方法构建了该系统的网络模型,这将允许在未来研究中根据需要进行进一步修改。该模型用于模拟机械负荷的影响以及不同干预措施的影响,例如连续或间歇给予PTH。我们的模型预测,缺乏规律的机械负荷和/或PTH昼夜节律受损会导致骨量随时间逐渐减少,通过模拟干预措施可以恢复,并且某些干预措施的有效性可能取决于其时机。