ArticleImmunity, inflammation and disease2025
Identification of Potential Common Pathogenic Mechanisms Underlying Osteoarthritis and Major Depressive Disorder Using Bioinformatics Analysis.
Article in Immunity, inflammation and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Identification of Potential Common Pathogenic Mechanisms Underlying Osteoarthritis and Major Depressive Disorder Using Bioinformatics Analysis.Immunity, inflammation and disease · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundPatients with osteoarthritis (OA) exhibit an elevated risk for major depressive disorder (MDD), primarily due to chronic pain and associated disability. However, the shared molecular mechanisms underlying these conditions remain poorly understood.
methodsThis study employs bioinformatics and systems biology approaches to identify common gene signatures and elucidate the shared pathogenesis of OA and MDD.
resultsWe identified 22 common differentially expressed genes between the two diseases, which were predominantly associated with the positive regulation of reactive oxygen species metabolic processes, immune and inflammatory responses, efferocytosis, the PI3K-Akt signaling pathway, the TGF-beta receptor signaling pathway, and immune system-related pathways. Notably, CXCR6, GZMK, and KLRG1 were identified as key genes, showing positive correlations with CD8+ T cells and negative correlations with naïve CD4+ T cells and monocytes in both OA and MDD. Competitive endogenous RNA regulatory network analysis revealed that the KCNQ1OT1-miR-92a/miR-132/miR-19b/miR-145-CXCR6/GZMK/KLRG1 and XIST1-miR-92a/miR-132/miR-19b-CXCR6/GZMK/KLRG1 regulatory axes may play critical roles in the pathogenesis of OA and MDD.
conclusionThese findings provide novel insights into the comorbidity mechanism of OA and MDD and may guide the development of individualized therapeutic strategies for patients with comorbid conditions.
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Registered trials
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