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 molecularmechanisms in accelerated aging SAMP6 mice

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 pathogenesis 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 mechanisms of SOP development and exploring its prevention and treatment.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 progression at both macroscopic and microscopic levels.