New Avenues in the LRP5-mediated Bone Mass Acquisition
Korean Journal of Bone Metabolism
;
: 1-9, 2012.
Artigo
em Coreano
| WPRIM
| ID: wpr-130877
ABSTRACT
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)beta-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 osteocyte-producing 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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Osteogênese
/
Osteoporose
/
Fenótipo
/
Dermatopatias
/
Triptofano
/
Triptofano Hidroxilase
/
Doenças Ósseas Metabólicas
/
Serotonina
/
Prolapso da Valva Mitral
/
Duodeno
Limite:
Animais
/
Humanos
Idioma:
Coreano
Revista:
Korean Journal of Bone Metabolism
Ano de publicação:
2012
Tipo de documento:
Artigo
Similares
MEDLINE
...
LILACS
LIS