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pmid:41503916

Identify Diagnostic Biomarkers Related to Taurine Metabolism in Diabetic Foot Ulcers Using Bulk RNA-seq and ScRNA-seq Analysis.

Mengrong He · Jiamin Chen

Journal of diabetes · 2026 doi:10.1111/1753-0407.70166

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:41503916
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science-record
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sha256:7d97744bf7abc7885827f4e8ed901e13914d344c8c970ced63770ffc386dc026
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2026-11-01T20:31:29Z
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2026-11-01T22:57:43Z
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title
Identify Diagnostic Biomarkers Related to Taurine Metabolism in Diabetic Foot Ulcers Using Bulk RNA-seq and ScRNA-seq Analysis.
doi
10.1111/1753-0407.70166
pmid
41503916
authors array · 2 items
[0]
Mengrong He
[1]
Jiamin Chen
journal
Journal of diabetes
year
2026
abstract
BACKGROUND: Diabetic foot ulcers (DFU) are severe complications with complex pathogenesis involving inflammation and impaired healing. Taurine, a key antioxidant amino acid, shows therapeutic potential in diabetes, but its role in DFU remains unclear and warrants investigation. METHODS: This integrated multi-omics study analyzed DFU using GEO transcriptomics data (training: GSE68183/GSE80178; validation: GSE37265/GSE134431; scRNA-seq: GSE223964). Limma identified DEGs that intersected with taurine metabolism -related genes. Key modules (MCODE) and a LASSO-based diagnostic signature were established. Immune infiltration was profiled via ssGSEA, CIBERSORT, and MCP-Counter. Regulatory networks (TFs/miRNAs) were predicted (miRNet/NetworkAnalyst), and therapeutic agents were screened (DSigDB). Seurat-processed scRNA-seq defined nine cell types, with CellChat analyzing intercellular communication. RESULTS: This study identified a three-gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near-perfect accuracy (training AUC = 1, validation AUC ≥ 0.98). Multi-omics analyses revealed significant immune dysregulation (increased B cells/CD8+T cells/M1 macrophages in DFS), collagen-centric signaling dominance, and two molecular subtypes. Single-cell RNA-seq uncovered cell-type-specific dysfunction: fibroblasts and endothelial cells expanded in DFS, while HMOX1 localized to Mono-macrophages and MAPK3 to endothelium. CONCLUSION: This study deeply analyzed DFU immune microenvironment characteristics, intercellular communication networks, and molecular regulatory mechanisms, revealing a dysregulated metabolic-immune repair network framework, providing new insights for understanding DFU pathological mechanisms and developing targeted diagnostic and therapeutic strategies.
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Differential analysis between the DFS and NFS was performed using the limma package with thresholds of adj.p.Val < 0.05 and |log2FC| > 0.585
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sections[5] "Differential Analysis and Identification of Key Modules" paragraph 2
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Differential analysis between the DFS and NFS was performed using the limma package with thresholds of adj.p.Val < 0.05 and |log2FC| > 0.585
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The data and materials in the current study are available from the corresponding author on reasonable request.
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This study identified a three-gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near-perfect accuracy, including a training AUC of 1 and validation AUCs of at least 0.98.
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This study identified a three‐gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near‐perfect accuracy (training AUC = 1, validation AUC ≥ 0.98).
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This study identified a three‐gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near‐perfect accuracy (training AUC = 1, validation AUC ≥ 0.98).
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This study identified a three-gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near-perfect accuracy, including a training AUC of 1 and validation AUCs of at least 0.98.
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Deregulated immune signature orchestrated by FOXM1 impairs human diabetic wound healing
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Gene expression profile as single cell level of chronic diabetic foot ulcers and chronic non-diabetic foot ulcer
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Comparative genomic, microRNA, and tissue analyses reveal subtle differences between non-diabetic and diabetic foot skin [gene expression]
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Genomic Profiling of Diabetic Foot Ulcers Identifies miR-15b-5p as a Major Regulator that Leads to Suboptimal Inflammatory Response and Diminished DNA Repair Mechanisms
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Differential analysis between the DFS and NFS was performed using the limma package with thresholds of adj.p.Val < 0.05 and |log2FC| > 0.585
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asset:data:geo:GSE37265 not downloaded
[6]
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[7]
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[8]
asset:data:geo:GSE80178 licence not read
[9]
asset:data:geo:GSE80178 not downloaded
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execution.not_run
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method.reader_differs_from_extractor
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review.human_critique
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review.independent_reader
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review.machine_critique
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confidence
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evidence array · 3 items
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etabolism in Diabetic Foot Ulcers Using Bulk RNA-seq and ScRNA-seq Analysis.
[1]
nce, and two molecular subtypes. Single-cell RNA-seq uncovered cell-type-specific dysfunction: fi
[2]
ted multi-omics study analyzed DFU using GEO transcriptomics data (training: GSE68183/GSE80178; validatio
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confidence
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evidence array · 4 items
[0]
Diabetic Foot Ulcers Using Bulk RNA-seq and ScRNA-seq Analysis.
[1]
aling dominance, and two molecular subtypes. Single-cell RNA-seq uncovered cell-type-specific dysfunction: fi
[2]
83/GSE80178; validation: GSE37265/GSE134431; scRNA-seq: GSE223964). Limma identified DEGs that inte
[3]
nts were screened (DSigDB). Seurat-processed scRNA-seq defined nine cell types, with CellChat analy
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Differential analysis between the DFS and NFS was performed using the limma package with thresholds of adj.p.Val < 0.05 and |log2FC| > 0.585
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Complete file
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Taurine, a key antioxidant amino acid, shows therapeutic potential in diabetes, but its role in DFU remains unclear and warrants investigation.\nMETHODS: This integrated multi-omics study analyzed DFU using GEO transcriptomics data (training: GSE68183/GSE80178; validation: GSE37265/GSE134431; scRNA-seq: GSE223964). Limma identified DEGs that intersected with taurine metabolism -related genes. Key modules (MCODE) and a LASSO-based diagnostic signature were established. Immune infiltration was profiled via ssGSEA, CIBERSORT, and MCP-Counter. Regulatory networks (TFs/miRNAs) were predicted (miRNet/NetworkAnalyst), and therapeutic agents were screened (DSigDB). Seurat-processed scRNA-seq defined nine cell types, with CellChat analyzing intercellular communication.\nRESULTS: This study identified a three-gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near-perfect accuracy (training AUC = 1, validation AUC ≥ 0.98). Multi-omics analyses revealed significant immune dysregulation (increased B cells/CD8+T cells/M1 macrophages in DFS), collagen-centric signaling dominance, and two molecular subtypes. Single-cell RNA-seq uncovered cell-type-specific dysfunction: fibroblasts and endothelial cells expanded in DFS, while HMOX1 localized to Mono-macrophages and MAPK3 to endothelium.\nCONCLUSION: This study deeply analyzed DFU immune microenvironment characteristics, intercellular communication networks, and molecular regulatory mechanisms, revealing a dysregulated metabolic-immune repair network framework, providing new insights for understanding DFU pathological mechanisms and developing targeted diagnostic and therapeutic strategies.", "claims": [{"id": "claim-method", "statement": "Differential analysis between the DFS and NFS was performed using the limma package with thresholds of adj.p.Val < 0.05 and |log2FC| > 0.585", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:41503916", "locator": "sections[5] \"Differential Analysis and Identification of Key Modules\" paragraph 2", "quote": "Differential analysis between the DFS and NFS was performed using the limma package with thresholds of adj.p.Val < 0.05 and |log2FC| > 0.585"}], "state": "complete"}, {"id": "claim-data-access", "statement": "The data and materials in the current study are available from the corresponding author on reasonable request.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:41503916", "locator": "sections[32] \"Data Availability Statement\" paragraph 2", "quote": "The data and materials in the current study are available from the corresponding author on reasonable request."}], "state": "complete"}, {"id": "claim-target-result", "statement": "This study identified a three-gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near-perfect accuracy, including a training AUC of 1 and validation AUCs of at least 0.98.", "kind": "quantitative", "target": {"value": 1.0, "unit": "auc", "tolerance": null, "source": "This study identified a three‐gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near‐perfect accuracy (training AUC = 1, validation AUC ≥ 0.98)."}, "evidence": [{"asset": "source:pmid:41503916", "locator": "sections[0] \"Abstract\" paragraph 3", "quote": "This study identified a three‐gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near‐perfect accuracy (training AUC = 1, validation AUC ≥ 0.98)."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "This study identified a three-gene diagnostic signature (HMOX1, MAPK3, TXN) for DFU with near-perfect accuracy, including a training AUC of 1 and validation AUCs of at least 0.98.", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:41503916"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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