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[骨免疫学:炎症如何影响骨代谢]

[Osteoimmunology: how inflammation influences bone metabolism].

作者信息

Lange U, Teichmann J, Schett G, Neumann E, Müller-Ladner U

机构信息

Professur für Internistische Rheumatologie, Osteologie, Physikalische Medizin der Universität Gießen; Kerckhoff-Klinik, Abteilung Rheumatologie, klinische Immunologie, Osteologie, Physikalische Medizin; Bad Nauheim.

出版信息

Dtsch Med Wochenschr. 2013 Sep;138(37):1845-9. doi: 10.1055/s-0033-1349486. Epub 2013 Sep 4.

Abstract

Bone remodelling is characterized by a balance between bone resorption and bone formation. The osteoblasts are responsible for bone synthesis and the osteoclasts for bone resorption. A finely adjusted interaction between molecular mechanisms leads, via cytokines, hormones and growth factors, to a homeostasis of the bone metabolism. Here, the RANK/RANKL/OPG-system is actively involved in the differentiation and function of osteoclasts and seems to play a central role in most pathophysiological mechanisms. An increased osteoclast activity results in inflammatory destructive manifestations and/or osteoporosis whereas an increased osteoblast activity can result in osteopetrosis. The present overview describes the known pathophysiological relevant metabolic pathways in this remodelling process especially the effect of inflammation on bone metabolism, and presents the links from bench to bedside.

摘要

骨重塑的特征是骨吸收与骨形成之间的平衡。成骨细胞负责骨合成,破骨细胞负责骨吸收。分子机制之间精细调节的相互作用通过细胞因子、激素和生长因子导致骨代谢的稳态。在此,RANK/RANKL/OPG系统积极参与破骨细胞的分化和功能,并且似乎在大多数病理生理机制中起核心作用。破骨细胞活性增加会导致炎症性破坏表现和/或骨质疏松症,而成骨细胞活性增加会导致骨质石化。本综述描述了该重塑过程中已知的与病理生理相关的代谢途径,尤其是炎症对骨代谢的影响,并展示了从实验室到临床的联系。

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