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关于《2015年骨质疏松症防治指南》。骨质疏松症的细胞机制与病因

[On "2015 Guidelines for Prevention and Treatment of Osteoporosis". Cellular mechanism and etiology of osteoporosis].

作者信息

Koga Takako, Takayanagi Hiroshi

机构信息

Department of Pharmacology, School of Dentistry, Showa University, Japan.

出版信息

Clin Calcium. 2015 Sep;25(9):1293-300.

PMID:26320528
Abstract

The bone is continuously renewed throughout adult life by the coordinated action of osteoclastic bone resorption and osteoblastic bone formation in response to various hormones, cytokines, chemokines and biomechanical external stimuli. This process, called bone remodeling, is a prerequisite for the normal bone homeostasis that maintains both bone quality and strength. An imbalance of bone resorption and bone formation is often central to metabolic bone diseases. Aging, various diseases including life-style-related diseases, and loss of mechanical stress lead to an excessive bone resorption, resulting in osteoporosis due to decreased bone mineral density and deterioration of bone quality. Therefore, the activity of both osteoclasts and osteoblasts must be tightly regulated during bone remodeling. Understanding the regulatory mechanisms of bone cells and signal transduction through bone cell communication is important for treating osteoporosis.

摘要

在成年期,骨骼通过破骨细胞的骨吸收和成骨细胞的骨形成的协同作用持续更新,以响应各种激素、细胞因子、趋化因子和生物力学外部刺激。这个过程称为骨重塑,是维持骨骼质量和强度的正常骨稳态的先决条件。骨吸收与骨形成的失衡通常是代谢性骨病的核心问题。衰老、包括生活方式相关疾病在内的各种疾病以及机械应力的丧失会导致骨吸收过度,由于骨矿物质密度降低和骨质量恶化而导致骨质疏松症。因此,在骨重塑过程中,破骨细胞和成骨细胞的活性都必须受到严格调节。了解骨细胞的调节机制以及通过骨细胞通讯进行的信号转导对于治疗骨质疏松症很重要。

相似文献

1
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引用本文的文献

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Risk Factors of Osteoporosis in Females: A Hospital-Based Case-Control Study, Yazd, Iran.伊朗亚兹德地区女性骨质疏松症的危险因素:一项基于医院的病例对照研究
Iran J Public Health. 2022 Jun;51(6):1371-1380. doi: 10.18502/ijph.v51i6.9693.
2
Tanshinone‑IIA attenuates the deleterious effects of oxidative stress in osteoporosis through the NF‑κB signaling pathway.丹参酮 IIA 通过 NF-κB 信号通路减轻骨质疏松症氧化应激的有害影响。
Mol Med Rep. 2018 May;17(5):6969-6976. doi: 10.3892/mmr.2018.8741. Epub 2018 Mar 14.