학술논문

快速老化SAMP6小鼠骨代谢及其分子机制研究进展 / Research progress on bone metabolism and molecular mechanisms in accelerated aging SAMP6 mice
Document Type
Academic Journal
Source
中国药理学通报 / Chinese Pharmacological Bulletin. 40(1):16-19
Subject
老年性骨质疏松
动物模型
快速老化小鼠P6品系
骨代谢
Wnt/β-catenin信号通路
功能分子
senile osteoporosis
animal models
senescence ac-celerated mouse prone 6
bone metabolism
Wnt/β-catenin sig-naling pathway
functional molecules
Language
Chinese
ISSN
1001-1978
Abstract
老年性骨质疏松(senile osteoporosis,SOP)是一种易发骨折的全身性骨病,发病过程复杂,机制研究不足.目前,快速老化小鼠 P6 品系(senescence accelerated mouse prone 6,SAMP6)是用于研究SOP发病机制和防治SOP的理想模型.该模型表现出骨脆性增加、骨微观结构退化、骨基质流失、骨内细胞代谢异常与功能紊乱等特征,从宏观到微观均能复制SOP发生和发展的过程.
Senile osteoporosis(SOP)is a systemic bone disease characterized by increased susceptibility to fractures.The patho-genesis of SOP is complex and not well understood.Currently,the rapid aging model mouse,senescence accelerated mouse prone 6(SAMP6),is an ideal model for studying the mecha-nisms of SOP development and exploring its prevention and treat-ment.This model exhibits characteristics including increased bone fragility,degradation of bone microstructure,loss of bone matrix,and abnormal metabolism and dysfunction of bone cells,faithfully replicating the process of SOP occurrence and progres-sion at both macroscopic and microscopic levels.