Regulation of Bone Mass by Serotonin: Molecular Biology and Therapeutic Implications

被引：55
作者：
Karsenty, Gerard [1 ]
Yaday, Vijay K. [2 ]
机构：
[1] Columbia Univ, Dept Genet & Dev, Med Ctr, New York, NY 10032 USA
[2] Wellcome Trust Sanger Inst, Mouse & Zebrafish Genet Grp, Cambridge CB10 1SA, England
来源：
ANNUAL REVIEW OF MEDICINE, VOL 62, 2011 | 2011年 / 62卷
关键词：
enterochromaffin cells; duodenum; Tph; 1; osteoblasts; proliferation; CREB; RECEPTOR-RELATED PROTEIN-5; LRP5; MUTATION; 11Q12-13;
D O I：
10.1146/annurev-med-090710-133426
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
The molecular elucidation of two human skeletal dysplasias revealed that they are caused by an increase or a decrease in the synthesis of serotonin by enterochromaffin cells of the gut. This observation revealed a novel and powerful endocrine means to regulate bone mass. Exploiting these findings in the pharmacological arena led to the demonstration that inhibiting synthesis of gut-derived serotonin could be an effective means to treat low-bone-mass diseases such as osteoporosis.
引用
收藏
页码：323 / 331
页数：9
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