ArticleFrontiers in neuroscience2022
Identification of the common differentially expressed genes and pathogenesis between neuropathic pain and aging.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
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- Locityper enables targeted genotyping of complex polymorphic genes.Nature genetics · 2025Article
- Unraveling the Disease Mechanisms of Neuropathic Pain Through Constructing miRNA-mRNA Networks Based on a Rat Model.Brain and behavior · 2025Article
- An in-depth understanding of the role and mechanisms of T cells in immune organ aging and age-related diseases.Science China. Life sciences · 2025Review
- Integrated bioinformatics analysis identified leucine rich repeat containing 15 and secreted phosphoprotein 1 as hub genes for calcific aortic valve disease and osteoarthritis.IET systems biology · 2024Article
- Age-associated changes in multimodal pain perception.Age and ageing · 2024Article
- Identification and validation of aging-related genes in neuropathic pain using bioinformatics.Frontiers in genetics · 2024Article
- Bioinformatics and systems biology approach to identify the pathogenetic link of neurological pain and major depressive disorder.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Unique miRomics Expression Profiles inInternational journal of molecular sciences · 2023Article
- Differentially Expressed Genes and Molecular Susceptibility to Human Age-Related Diseases.International journal of molecular sciences · 2023Article
- Mechanism of ERK/CREB pathway in pain and analgesia.Frontiers in molecular neuroscience · 2023Review
- A Deep Differential Analysis in Four Subtypes of Breast Cancer Based on Regulations of miRNA-mRNA.IET systems biologyArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Neuropathic pain is a debilitating disease caused by damage or diseases of the somatosensory nervous system. Previous research has indicated potential associations between neuropathic pain and aging. However, the mechanisms by which they are interconnected remain unclear. In this study, we aim to identify the common differentially expressed genes (co-DEGs) between neuropathic pain and aging through integrated bioinformatics methods and further explore the underlying molecular mechanisms. Methods: The microarray datasets GSE24982, GSE63442, and GSE63651 were downloaded from Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and co-DEGs were first identified. Functional enrichment analyses, protein-protein Interaction (PPI) network, module construction and hub genes identification were performed. Immune infiltration analysis was conducted. Targeted transcription factors (TFs), microRNAs (miRNAs) and potential effective drug compounds for hub genes were also predicted. Results: A total of 563 and 1,250 DEGs of neuropathic pain and aging were screened, respectively. 16 genes were further identified as co-DEGs. The functional analysis emphasizes the vital roles of the humoral immune response and complement and coagulation cascades in these two diseases. Cxcl14, Fblim1, RT1-Da, Serping1, Cfd, and Fcgr2b were identified as hub genes. Activated B cell, mast cell, activated dendritic cell, CD56 bright natural killer cell, effector memory CD8 + T cell, and type 2 T helper cell were significantly up-regulated in the pain and aging condition. Importantly, hub genes were found to correlate with the activated B cell, activated dendritic cell, Gamma delta T cell, central memory CD4 + T cell and mast cell in pain and aging diseases. Finally, Spic, miR-883-5p, and miR-363-5p et al. were predicted as the potential vital regulators for hub genes. Aldesleukin, Valziflocept, MGD-010, Cinryze, and Rhucin were the potential effective drugs in neuropathic pain and aging. Conclusion: This study identified co-DEGs, revealed molecular mechanisms, demonstrated the immune microenvironment, and predicted the possible TFs, miRNAs regulation networks and new drug targets for neuropathic pain and aging, providing novel insights into further research.
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