Oxidative Stress and Intervertebral Disc Degeneration: Pathophysiology, Signaling Pathway, and Therapy

被引:33
|
作者
Li, Yanrun [1 ]
Chen, Lu [2 ]
Gao, Yu [1 ]
Zou, Xuenong [3 ]
Wei, Fuxin [1 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 7, Dept Orthopaed Surg, Shenzhen 518170, Peoples R China
[2] Jinan Univ, Dept Med Ultrason, Affiliated Hosp 1, Guangzhou 510070, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Spinal Surg, Guangdong Prov Key Lab Orthoped & Traumatol, Guangzhou 510080, Peoples R China
基金
中国国家自然科学基金;
关键词
NF-KAPPA-B; NUCLEUS PULPOSUS CELLS; VERTEBRAL END-PLATE; MAGNETIC-RESONANCE; EXTRACELLULAR-MATRIX; INFLAMMATION; SENESCENCE; APOPTOSIS; AUTOPHAGY; MITOCHONDRIA;
D O I
10.1155/2022/1984742
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Intervertebral disc degeneration (IDD), characterized as decreased proteoglycan content, ossification of endplate, and decreased intervertebral height, is one of the major reasons of low back pain, which seriously affects the quality of life and also brings heavy economic burden. However, the mechanisms leading to IDD and its therapeutic targets have not been fully elucidated. Oxidative stress refers to the imbalance between oxidation and antioxidant systems, between too many products of reactive oxygen species (ROS) and the insufficient scavenging function. Excessive ROS can damage cell lipids, nucleic acids and proteins, which has been proved to be related to the development of a variety of diseases. In recent years, an increasing number of studies have reported that oxidative stress is involved in the pathological process of IDD. Excessive ROS can accelerate the IDD process via inducing the pathological activities, such as inflammation, apoptosis, and senescence. In this review, we focused on pathophysiology and molecular mechanisms of oxidative stress-induced IDD. Moreover, the present review also summarized the possible ideas for the future therapy strategies of oxidative stress-related IDD.
引用
收藏
页数:14
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