ArticleFrontiers in immunology2023
Revealing the roles of glycosphingolipid metabolism pathway in the development of keloid: a conjoint analysis of single-cell and machine learning.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 19 citations in OpenAlex.
- Predictive and mechanistic insights ofPeerJ · 2026Article
- A panoramic analysis of keloid pathogenesis: multidimensional network regulation of genetics-immunity-metabolism-mechanical force.Frontiers in immunology · 2026Review
- Article
- 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
- Globotriaosylceramide Gb3 Influences Wound Healing and Scar Formation by Orchestrating Fibroblast Heterogeneity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Uncovering a fibroblast differentiation-based keloid classification by integration of single-cell and bulk RNA sequencing.Communications biology · 2025Article
- Identification of potential biomarkers and mechanisms for keloid disorder based on comprehensive bioinformatics analysis and machine learning algorithms.BMC medical genomics · 2025Article
- Effects of exosomes from human dental pulp stem cells on the biological behavior of human fibroblasts.Scientific reports · 2025Article
- Exploring machine learning strategies for single-cell transcriptomic analysis in wound healing.Burns & trauma · 2025Review
- Glycosphingolipids in Cardiovascular Disease: Insights from Molecular Mechanisms and Heart Failure Models.Biomolecules · 2024Review
- Article
- Myofibroblasts reside in the middle dermis of the keloids but do not predict the response to injection therapies: a double-blinded, randomized, controlled trial.Frontiers in medicine · 2024Article
- Deciphering the contributions of cuproptosis in the development of hypertrophic scar using single-cell analysis and machine learning techniques.Frontiers in immunology · 2023Article
- Uncovering the immune microenvironment and molecular subtypes of hepatitis B-related liver cirrhosis and developing stable a diagnostic differential model by machine learning and artificial neural networks.Frontiers in molecular biosciences · 2023Article
- Betanin Promotes Wound Closure and Drives a Context-Specific Transcriptional Repair Program in HaCaT Keratinocytes: A Multi-Evidence AI-Guided Prioritization Study.BioFactors (Oxford, England)Article
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11 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Keloid is a pathological scar formed by abnormal wound healing, characterized by the persistence of local inflammation and excessive collagen deposition, where the intensity of inflammation is positively correlated with the size of the scar formation. The pathophysiological mechanisms underlying keloid formation are unclear, and keloid remains a therapeutic challenge in clinical practice. This study is the first to investigate the role of glycosphingolipid (GSL) metabolism pathway in the development of keloid. Single cell sequencing and microarray data were applied to systematically analyze and screen the glycosphingolipid metabolism related genes using differential gene analysis and machine learning algorithms (random forest and support vector machine), and a set of genes, including ARSA,GBA2,SUMF2,GLTP,GALC and HEXB, were finally identified, for which keloid diagnostic model was constructed and immune infiltration profiles were analyzed, demonstrating that this set of genes could serve as a new therapeutic target for keloid. Further unsupervised clustering was performed by using expression profiles of glycosphingolipid metabolism genes to discover keloid subgroups, immune cells, inflammatory factor differences and the main pathways of enrichment between different subgroups were calculated. The single-cell resolution transcriptome landscape concentrated on fibroblasts. By calculating the activity of the GSL metabolism pathway for each fibroblast, we investigated the activity changes of GSL metabolism pathway in fibroblasts using pseudotime trajectory analysis and found that the increased activity of the GSL metabolism pathway was associated with fibroblast differentiation. Subsequent analysis of the cellular communication network revealed the existence of a fibroblast-centered communication regulatory network in keloids and that the activity of the GSL metabolism pathway in fibroblasts has an impact on cellular communication. This contributes to the further understanding of the pathogenesis of keloids. Overall, we provide new insights into the pathophysiological mechanisms of keloids, and our results may provide new ideas for the diagnosis and treatment of keloids.
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