ArticleFrontiers in immunology2022
Identification and characterization of four immune-related signatures in keloid.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Efficacy and Safety of Pressure Therapy Alone and in Combination with Silicone in Prevention of Hypertrophic Scars: A Systematic Review with Meta-analysis of Randomized Controlled Trials.Aesthetic plastic surgery · 2023Pooled it
- LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.Lasers in surgery and medicine · 2026Article
- Integrative Transcriptomic and Machine Learning Analysis Identifies JAG1 and NR2F2 in Keloid.Clinical, cosmetic and investigational dermatology · 2026Article
- Identification and Preliminary mRNA Validation of Key Genes Associated with Tolerogenic Dendritic Cells in Keloid Based on Transcriptome Data.Clinical, cosmetic and investigational dermatology · 2026Article
- Mesenchymal stem cells attenuate keloid pathogenesis via TGF-β1/SMAD-driven MMP9 suppression: mechanistic insights into collagen remodeling and extracellular matrix homeostasis.Blood science (Baltimore, Md.) · 2025Article
- Identification and Analysis of Immune Microenvironment-Related Genes for Keloid Risk Prediction and Their Effects on Keloid Proliferation and Migration.Biochemical genetics · 2024Article
- Commensal microbiome dysbiosis elicits interleukin-8 signaling to drive fibrotic skin disease.PNAS nexus · 2024Article
- Scars.Nature reviews. Disease primers · 2023Review
- The functions and clinical application potential of exosomes derived from mesenchymal stem cells on wound repair: a review of recent research advances.Frontiers in immunology · 2023Review
- Multimodal roles of transient receptor potential channel activation in inducing pathological tissue scarification.Frontiers in immunology · 2023Review
- Decoding the molecular landscape of keloids: new insights from single-cell transcriptomics.Burns & trauma · 2023Review
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A keloid is a fibroproliferative disorder of unknown etiopathogenesis that requires ill-defined treatment. Existing evidence indicates that the immune system plays an important role in the occurrence and development of keloid. However, there is still a lack of research on the immune-related signatures of keloid. Here we identified immune-related signatures in keloid and explored their pathological mechanisms. Transcriptomic datasets (GSE7890, GSE92566, and GSE44270) of keloid and normal skin tissues were obtained from the Gene Expression Omnibus database. The overlap of differentially expressed genes and immune-related genes was considered as differentially expressed immune-related genes (DEIGs). Functional analysis, expression, and distribution were applied to explore the function and characteristics of DEIGs, and the expression of these DEIGs in keloid and normal skin tissues was verified by immunohistochemistry. Finally, we conducted interactive network analysis and immune infiltration analysis to determine the therapeutic potential and immune correlation. We identified four DEIGs (LGR5, PTN, JAG1, and DKK1). In these datasets, only GSE7890 met the screening criteria. In the GSE7890 dataset, DKK1 and PTN were downregulated in keloid, whereas JAG1 and LGR5 were upregulated in keloid. In addition, we obtained the same conclusion through immunohistochemistry. Functional analysis indicated that these four DEIGs were mainly involved in stem cell, cell cycle, UV response, and therapy resistance. Through interactive network analysis, we found that these DEIGs were associated with drugs currently used to treat keloid, such as hydrocortisone, androstanolone, irinotecan, oxaliplatin, BHQ-880, and lecoleucovorin. Finally, many immune cells, including CD8
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