The Time Course Pathological Changes After Burn Injury
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Updated: Feb 8, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
Dan Wu1,2, Ming Zhou3, Liang Li2
1Department of Plastic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, 266003, Shandong, China.
Abstract:
In the present study, we aimed to explore the time course pathological changes after burn injury. The time course microarray data of burn injury from the Gene Expression Omnibus (GEO) was further analyzed through bioinformatics analysis. The differential expression genes (DEGs) were identified in the early-stage vs. control groups, middle-stage vs. control groups, and early-stage vs. middle-stage groups after burn injury, followed by pathway enrichment analysis. Gene modules associated with burn injury progression were identified through weighted gene co-expression network analysis (WGCNA), and hub genes were identified via network topology analysis. There were a total of 745 DEGs in the early vs. control group, 1104 DEGs in mid vs. control, and 61 DEGs in early vs. mid group. The significant pathways enriched by DEGs in the middle stage were also enriched by DEGs in the early stage. Immunodeficiency was a significant pathway specific for the DEGs in the early stage. There were 19 overlapped genes, such as myeloperoxidase, transcobalamin, and interferon-induced protein with tetratricopeptide repeats 1, among DEGs in early vs. control, middle vs. control, and early vs. middle groups. WGCNA identified three gene modules that were significantly associated with burn injury progression. Furthermore, we identified several gene modules and biological processes that might be associated with burn injury progression, and such results may be beneficial in understanding the underlying mechanisms and developing novel drugs.
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