ArticleInternational wound journal2024
Identification and clinical validation of the role of anoikis-related genes in diabetic foot.
Article in International wound journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Overexpression of Neural Precursor Cell Expressed Developmentally Downregulated 9 (NEDD9) reduces ox-LDL-induced Anoikis in atherosclerotic vascular endothelial cells.International journal of cardiology. Heart & vasculature · 2025Article
- LncRNA and mRNA expression characteristic and bioinformatic analysis in anemic diabetic foot ulcers.Frontiers in genetics · 2025Article
- Article
- Identification and clinical validation of the role of anoikis-related genes in diabetic foot.International wound journal · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
This study aims to investigate the role of anoikis-related genes in diabetic foot (DF) by utilizing bioinformatics analysis to identify key genes associated with anoikis in DF. We selected the GEO datasets GSE7014, GSE80178 and GSE68183 for the extraction and analysis of differentially expressed anoikis-related genes (DE-ARGs). GO analysis and KEGG analysis indicated that DE-ARGs in DF were primarily enriched in apoptosis, positive regulation of MAPK cascade, anoikis, focal adhesion and the PI3K-Akt signalling pathway. Based on the LASSO and SVM-RFE algorithms, we identified six characteristic genes. ROC curve analysis revealed that these six characteristic genes had an area under the curve (AUC) greater than 0.7, indicating good diagnostic efficacy. Expression analysis in the validation set revealed downregulation of CALR in DF, consistent with the training set results. GSEA results demonstrated that CALR was mainly enriched in blood vessel morphogenesis, endothelial cell migration, ECM-receptor interaction and focal adhesion. The HPA database revealed that CALR was moderately enriched in endothelial cells, and CALR was found to interact with 63 protein-coding genes. Functional analysis with DAVID suggested that CALR and associated genes were enriched in the phagosome component. CALR shows promise as a potential marker for the development and treatment of DF.
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Registered trials
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