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JAK-STAT与骨代谢

JAK-STAT and bone metabolism.

作者信息

Li Jiliang

机构信息

Department of Biology; Indiana University Purdue University Indianapolis; Indianapolis, IN USA.

出版信息

JAKSTAT. 2013 Jul 1;2(3):e23930. doi: 10.4161/jkst.23930. Epub 2013 Aug 15.

DOI:10.4161/jkst.23930
PMID:24069548
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3772100/
Abstract

Emerging evidences suggest Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway plays an important role in bone development and metabolism. Effects of JAK-STAT pathway on skeletal development are summarized based on skeletal phenotype of individual JAK and STAT gene knockout mouse. Furthermore, STAT3 has more profound effects on bone homeostasis compared with the other STATs. STAT3 mutation causes a disease called Job syndrome, most patients with which have associated craniofacial and skeletal features. Selective inactivation of STAT3 in osteoblasts decreases bone formation and skeletal responsiveness to mechanical loading. Future research includes investigating JAK-STAT signaling in osteoclasts and osteocytes.

摘要

新出现的证据表明，Janus激酶（JAK）-信号转导及转录激活因子（STAT）信号通路在骨骼发育和代谢中起重要作用。基于单个JAK和STAT基因敲除小鼠的骨骼表型，总结了JAK-STAT通路对骨骼发育的影响。此外，与其他STATs相比，STAT3对骨稳态的影响更为深远。STAT3突变会导致一种名为Job综合征的疾病，大多数患者伴有颅面和骨骼特征。成骨细胞中STAT3的选择性失活会减少骨形成以及骨骼对机械负荷的反应。未来的研究包括研究破骨细胞和骨细胞中的JAK-STAT信号传导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/b4a782e836fc/jkst-2-e23930-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/437983035012/jkst-2-e23930-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/0618ff4d5141/jkst-2-e23930-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/b4a782e836fc/jkst-2-e23930-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/437983035012/jkst-2-e23930-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/0618ff4d5141/jkst-2-e23930-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efa/3772100/b4a782e836fc/jkst-2-e23930-g3.jpg

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