ArticleBiochemical genetics2024
Mitochondria-Related Gene MAOB is a Key Biomarker of Osteoarthritis and Inhibition of Its Expression Reduces LPS-induced Chondrocyte Damage.
Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Exploration of acetylation-related biomarkers in osteoarthritis through bioinformatics analysis.PloS one · 2026Article
- Deciphering key chemotherapeutic drug targets within tyrosine metabolism for breast cancer and advancing a wide-ranging diagnostic strategy.Discover oncology · 2025Article
- The metabolites of gut microbiota: their role in ferroptosis in inflammatory bowel disease.European journal of medical research · 2025Review
- Identification of a novel disulfidptosis-related gene signature in osteoarthritis using bioinformatics analysis and experimental validation.Scientific reports · 2025Article
- Novel Insights into the Regulatory Role of N6-Methyladenosine in the Pathogenesis and Clinical Treatment of Osteoarthritis: Research Status and Prospect.Journal of inflammation research · 2025Review
- Identification of genetic association between mitochondrial dysfunction and knee osteoarthritis through integrating multi-omics: a summary data-based Mendelian randomization study.Clinical rheumatology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The mitochondria are an important organelle in cells responsible for producing energy, and its abnormal function is closely related to the occurrence and development of osteoarthritis. Finding key genes associated with mitochondrial dysfunction in osteoarthritis can provide new ideas for the study of its pathogenesis. Firstly, 371 differential expressed genes (DEGs) were obtained through bioinformatics analysis of the GSE12021 and GSE55235 datasets in the GEO database, and 24 mitochondria-related DEGs (Mito-DEGs) were obtained by crossing differential genes with mitochondrial related genes. Next, KEGG and GO analysis of Mito-DEGs showed that upregulated Mito-DEGs were mainly enriched in small molecule catabolic process and tryptophan metabolism, while downregulated Mito-DEGs were mainly enriched in acetyl-CoA metabolic process and fatty acid biosynthesis. Furthermore, the key genes ME2 and MAOB were obtained through protein-protein interaction network analysis and lasso cox analysis of the 24 Mito-DEGs. In addition, the comparison results of immune cell scores showed differences between T cells CD4 memory resting, T cells regulatory (Tregs), Mast cells resting, and Mast cells activated in the OA group and the control group. More importantly, the potential regulatory mechanisms of key genes were studied through GSEA analysis and their correlation with immune infiltrating cells, immune checkpoints, m6A, and ferroptosis. Finally, in LPS-induced C28/I2 cells, silencing MAOB reduced inflammation injury and inhibited mitochondrial damage. Our research findings suggest that MAOB may hold potential as a target for the diagnosis and treatment of osteoarthritis.
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Registered trials
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