Oxidative Stress in Intervertebral Disc Degeneration: New Insights from Bioinformatic Strategies

被引:11
|
作者
Zhao, Yongzhao [1 ,2 ,3 ]
Xiang, Qian [1 ,2 ,3 ]
Lin, Jialiang [1 ,2 ,3 ]
Jiang, Shuai [1 ,2 ,3 ]
Li, Weishi [1 ,2 ,3 ]
机构
[1] Peking Univ Third Hosp, Dept Orthopaed, Beijing, Peoples R China
[2] Beijing Key Lab Spinal Dis Res, Beijing, Peoples R China
[3] Minist Educ, Engn Res Ctr Bone & Joint Precis Med, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
NUCLEUS PULPOSUS CELLS; APOPTOSIS; AUTOPHAGY; INHIBITION; ACTIVATION; EXPRESSION; PROMOTES; TARGETS;
D O I
10.1155/2022/2239770
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oxidative stress has been proved to play important roles in the development of intervertebral disc degeneration (IDD); however, the underlying mechanism remains obscure to date. The aim of this study was to elucidate the vital roles of oxidative stress-related genes in the development of IDD using strict bioinformatic algorithms. The microarray data relevant to the IDD was downloaded from Gene Expression Omnibus database for further analysis. A series of bioinformatic strategies were used to determine the oxidative stress-related and IDD-related genes (OSIDDRGs), perform the function enrichment analysis and protein-protein interaction analysis, construct the lncRNA-miRNA-mRNA regulatory network, and investigate the potential relationship of oxidative stress to immunity abnormality and autophagy in IDD. We observed a significantly different status of oxidative stress between normal intervertebral disc tissues and IDD tissues. A total of 72 OSIDDRGs were screened out for the further function enrichment analysis, and 10 hub OSIDDRGs were selected to construct the lncRNA-miRNA-mRNA regulatory network. There was a very close association of oxidative stress with immunity abnormality and autophagy in IDD. Taken together, our findings can provide new insights into the mechanism research of oxidative stress in the development of IDD and offer new potential targets for the treatment strategies.
引用
收藏
页数:27
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