Yuan Feng-Lai, Xu Ming-Hui, Li Xia, Xinlong He, Fang Wei, Dong Jian
Department of Orthopaedics and Central Laboratory, The Third Hospital Affiliated to Nantong University Wuxi, China.
Department of Neurosurgery, Wuxi Ninth People's Hospital Affiliated to Soochow University Liangxi Road Wuxi, China.
Front Physiol. 2016 Jun 24;7:222. doi: 10.3389/fphys.2016.00222. eCollection 2016.
The adverse effect of acidosis on the skeletal system has been recognized for almost a century. Although the underlying mechanism has not been fully elucidated, it appears that acidosis acts as a general stimulator of osteoclasts derived from bone marrow precursors cells and enhances osteoclastic resorption. Prior work suggests that acidosis plays a significant role in osteoclasts formation and activation via up-regulating various genes responsible for its adhesion, migration, survival and bone matrix degradation. Understanding the role of acidosis in osteoclast biology may lead to development of novel therapeutic approaches for the treatment of diseases related to low bone mass. In this review, we aim to discuss the recent investigations into the effects of acidosis in osteoclast biology and the acid-sensing molecular mechanism.
酸中毒对骨骼系统的不良影响已被认识近一个世纪。尽管其潜在机制尚未完全阐明，但酸中毒似乎是骨髓前体细胞来源的破骨细胞的一般刺激物，并增强破骨细胞的吸收作用。先前的研究表明，酸中毒通过上调负责其黏附、迁移、存活和骨基质降解的各种基因，在破骨细胞的形成和激活中起重要作用。了解酸中毒在破骨细胞生物学中的作用可能会导致开发出治疗低骨量相关疾病的新治疗方法。在这篇综述中，我们旨在讨论最近关于酸中毒对破骨细胞生物学影响及酸敏感分子机制的研究。
