| New Avenues in the LRP5-mediated Bone Mass Acquisition |
| LRP5와 골량 획득의 새로운 지평 |
| 최제용 |
| 경북대학교 의학전문대학원 |
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| Abstract |
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Lipoprotein receptor-related protein (LRP5) signaling is well correlated with the bone mass in both human and mice.
Loss-of-function mutations of LRP5 result in osteopenia or osteoporosis. In contrast, gain-of-function mutations show
high bone mass phenotype. To elucidate the molecular mechanism of the LRP5-mediated bone mass acquisition, several
groups have genetically dissected the Wingless and Int-1 (Wnt) -catenin signaling pathway using osteoblast-lineage
specific Cre mice. Key players for LRP5-mediated bone mass acquisition turn out to be different molecules with
respect to the expressing tissue and action mode of these molecules. One is serotonin, a tryptophan metabolite that
originates from duodenum, which acts as a negative regulator for bone formation. LRP5 suppresses serotonin
biosynthesis by inhibiting the expression of tryptophan hydroxylase 1 in the gut. The other is sclerostin, an osteocyteproducing
antagonist for LRP5 signaling. Here is a summary of recent findings about these two molecules, providing
a chance to speculate new avenues in the LRP5-mediated bone mass acquisition. |
| Key Words:
Bone mass, LRP5, Sclerostin, Serotonin, Wnt signaling |
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