摘要
椎间盘退行性变(intervertebral disc degeneration,IDD)是多种慢性脊椎疾病的主要致病因素,其主要临床症状包括下腰痛和急性下肢神经根性疼痛。近年来,随着人口老龄化进展加速及生活方式改变,IDD的发病率显著上升且呈现年轻化趋势,严重影响了患者的生活质量,并给社会带来了巨大的经济和医疗负担。如何有效防治IDD已成为当前亟待解决的医学难题。现有研究表明,椎间盘细胞衰老在IDD的发生与进展中扮演着重要角色,靶向衰老椎间盘细胞的治疗策略,如抗细胞衰老药物、基因编辑及干细胞疗法等,正逐渐成为研究热点。该文综述了椎间盘细胞衰老的分子机制,阐述了针对衰老细胞的多种治疗策略及最新进展,旨在为IDD的防治提供新的研究思路和治疗靶点,并为后续研究提供参考。
Intervertebral disc degeneration(IDD)is the primary etiology of various chronic spinal disorders,characterized by clinical symptoms including low back pain and acute lower limb radicular pain.In recent years,due to accelerated population aging and lifestyle changes,there has been a significant increase in the incidence of IDD,particularly among younger individuals.This not only severely impacts patients'quality of life but also imposes substantial economic and medical burdens on society.Consequently,effective prevention and treatment strategies for IDD have become urgent medical priorities.Previous studies have demonstrated that cellular senescence of interverte-bral disc cells plays a crucial role in the initiation and progression of IDD.As such,therapeutic interventions target-ing senescent intervertebral disc cells,such as anti-senescence drugs,gene editing techniques,and stem cell therapy,are emerging as promising research areas.This review article comprehensively explores the molecular mechanisms underlying cellular senescence in IDD while discussing diverse therapeutic approaches and their latest advancements pertaining to senescent cells.The aim is to provide novel research insights and potential therapeutic targets for preventing and treating IDD while offering valuable references for future investigations.
作者
靳级
孙红
庄勇
宁旭
刘淼
JIN Ji;SUN Hong;ZHUANG Yong;NING Xu;LIU Miao(Department of Orthopaedics,Affiliated Hospital of Guizhou Medical University,Guiyang 550004,Guizhou,China;School of Clinical Medicine,Guizhou Medical University,Guiyang 550004,Guizhou,China;不详)
出处
《实用医学杂志》
CAS
北大核心
2024年第22期3268-3274,共7页
The Journal of Practical Medicine
基金
贵州省科技厅基础研究计划(编号:黔科合基础-ZK[2022]一般430)。
