Caltrin as a calcium transport inhibitor during osteoclastic bone resorption

在骨质疏松症、Paget病和关节炎等许多常见的骨病中都观察到了过度的骨吸收。这些都是澳大利亚和其他发达国家的主要健康问题。破骨细胞的激活或形成增加是导致过度骨吸收的原因。了解破骨细胞发挥功能和激活的机制是制定治疗和预防溶骨性疾病的过度骨吸收策略的重要一步。该项目试图解决破骨细胞功能这一重要而基本的问题。我们已经确定了Caltrin，一种已知的钙转运抑制剂，可能在破骨细胞钙稳态中具有重要的生物学意义。本项目旨在研究钙蛋白在钙诱导的细胞凋亡、破骨细胞骨吸收中的作用及其所强调的细胞和分子机制。这将增强我们对破骨细胞钙调节的了解，并为开发新的抗吸收药物提供信息。

Excessive bone resorption has been observed in many common bone diseases such as osteoporosis, Paget's disease and arthritis. These are major health problems in Australia and other developed countries. Increased activation or formation of osteoclasts is responsible for the excessive bone resorption. Understanding the mechanisms by which the osteoclasts exert its function and activation is an important step toward developing strategies to combat excessive bone resorption for the treatment and prevention of osteolytic disorders. This project attempts to address the important and fundamental issue of osteoclast function. We have identified caltrin, a known calcium transport inhibitor, that is likely to be biologically important in osteoclast calcium homeostasis. This project intends to investigate the role of caltrin in calcium-induced apoptosis, osteoclast bone resorption and the cellular and molecular mechanisms underlined. It will enhance our knowledge of calcium regulation in osteoclasts and provide information to facilitate the development of new anti-resorptive agents.