快速老化SAMP6小鼠骨代谢及其分子机制研究进展OACSTPCD
Research progress on bone metabolism and molecular mechanisms 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 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.
马绍勇;杨梦;王佳佳;杨亚军
广东医科大学药理学教研室,广东天然药物研究与开发重点实验室,广东湛江 524023
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 osteoporosisanimal modelssenescence ac-celerated mouse prone 6bone metabolismWnt/β-catenin sig-naling pathwayfunctional molecules
《中国药理学通报》 2024 (001)
16-19 / 4
国家自然科学基金资助项目(No 82274614)
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