详细信息

程序性细胞死亡对骨关节炎软骨基质稳态的影响    

The effect of programmed cell death on cartilage matrix homeostasis in osteoarthritis

文献类型:期刊文献

中文题名:程序性细胞死亡对骨关节炎软骨基质稳态的影响

英文题名:The effect of programmed cell death on cartilage matrix homeostasis in osteoarthritis

作者:刘建军[1];齐伟[2];安文博[1];陈欣[1];胡紫阳[2];马姣姣[2];陈一新[2];齐鑫[2]

第一作者:刘建军

机构:[1]甘肃中医药大学附属医院,兰州730000;[2]甘肃中医药大学,兰州730000

第一机构:甘肃中医药大学第二附属医院

年份:2024

卷号:33

期号:2

起止页码:184

中文期刊名:中国组织化学与细胞化学杂志

外文期刊名:Chinese Journal of Histochemistry and Cytochemistry

收录:CSTPCD;;CSCD:【CSCD_E2023_2024】;

基金:2022年兰州市科技局科技计划(2022-3-28);2021兰州市科技局指导性计划项目(2022-2D-91);2022年甘肃省科技厅省级科技计划(22JR11RA126);2022年甘肃省中医药科研项目(GZKZ-2022-4)。

语种:中文

中文关键词:骨关节炎;细胞程序性死亡;软骨基质

外文关键词:Osteoarthritis;programmed cell death;cartilage matrix

摘要:骨关节炎(osteoarthritis,OA)为软骨退行性变为主要病理特征,是中老年患者关节疼痛、肢体残疾、生活质量降低的主要病症,其发病机制尚未完全阐明,目前临床尚无根治方法。软骨细胞外基质的破坏和异常稳态作为OA的标志和软骨再生的治疗靶点,越来越受到人们的重视。细胞程序性死亡是指为保持内环境稳定,由基因主导的细胞自主有序性死亡。已证实,细胞程序性死亡作用下软骨代谢稳态失衡和骨关节炎发生发展密切相关。本文总结细胞程序性死亡对骨关节炎软骨基质稳态的影响及可能的影响途径,不同死亡模式对软骨基质稳态的调控方式、影响特点。
Osteoarthritis(OA)is primarily characterized by degenerative changes in cartilage and is a major cause of joint pain,physical disability,and reduced quality of life in middle-aged and elderly patients.The pathogenesis of OA has not been fully elucidated,and there are currently no curative treatments available.The destruction of the extracellular matrix of cartilage and abnormal homeostasis are recognized as hallmarks of OA and targets for cartilage regeneration therapies,increasingly gaining attention.Programmed cell death refers to the genetically regulated,orderly,and autonomous death of cells to maintain internal stability.It has been confirmed that programmed cell death is closely related to the imbalance in cartilage metabolic homeostasis and the development of osteoarthritis.This article summarizes the impact of programmed cell death on the homeostasis of the cartilage matrix in osteoarthritis and possible pathways of influence,as well as the regulatory mechanisms and distinctive effects of different modes of cell death on cartilage matrix homeostasis.

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