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The roles of the sympathetic nervous system in osteoporotic diseases: A review of experimental and clinical studies

期刊

AGEING RESEARCH REVIEWS
卷 10, 期 2, 页码 253-263

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2011.01.002

关键词

Osteoporotic disease; Bone remodeling; Sympathetic nervous system; Adrenergic signaling; Neurotransmitter

资金

  1. National Natural Science Foundation of China [U1032001, 81000779]
  2. Science and Technology Commission of the Shanghai Municipality [08411950100]

向作者/读者索取更多资源

With the rapid aging of the world population, the issue of skeletal health is becoming more prominent and urgent. The bone remodeling mechanism has sparked great interest among bone research societies. At the same time, increasing clinical and experimental evidence has driven attention towards the pivotal role of the sympathetic nervous system (SNS) in bone remodeling. Bone remodeling is thought to be partially controlled by the hypothalamus, a process which is mediated by the adrenergic nerves and neurotransmitters. Currently, new knowledge about the role of the SNS in the development and pathophysiology of osteoporosis is being generated. The aim of this review is to summarize the evidence that proves the involvement of the SNS in bone metabolism and to outline some common osteoporotic diseases that occur under different circumstances. The adrenergic signaling pathway and its neurotransmitters are involved to various degrees of importance in the development of osteoporosis in postmenopause, as well as in spinal cord injury, depression, unloading and the complex regional pain syndrome. In addition, clinical and pharmacological studies have helped to increase the comprehension of the adrenergic signaling pathway. We try to individually examine the contributions of the SNS in osteoporotic diseases from a different perspective. It is our hope that a further understanding of the adrenergic signaling by the SNS will pave the way for conceptualizing optimal treatment regimens for osteoporosis in the near future. (C) 2011 Elsevier B.V. All rights reserved.

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