ArticleInternational wound journal2023
Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid.
Article in International wound journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- A fibroblast-dependent TGF-β1/sFRP2 noncanonical Wnt signaling axis promotes epithelial metaplasia in idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2024Trial
- POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).Molecular medicine reports · 2026Review
- Identification and Verification of SLC6A15 Involved in Keloid via Bioinformatics Analysis and Machine Learning.Biochemical genetics · 2026Article
- A panoramic analysis of keloid pathogenesis: multidimensional network regulation of genetics-immunity-metabolism-mechanical force.Frontiers in immunology · 2026Review
- MicroRNAs in thyroid eye disease: expression signatures and clinical implications.Frontiers in immunology · 2026Review
- Regulatory role of POSTN in keloid pathogenesis.Molecular medicine reports · 2025Article
- Fibrotic Disease of the Skin and Lung: Shared Pathways, Environmental Drivers, and Therapeutic Opportunities in a Changing Climate.International journal of molecular sciences · 2025Review
- Discovery Potential Hub Genes and Pathways in Keloid Fibroblast Development Based on Bioinformatics Analysis.International journal of genomics · 2025Article
- Periostin regulates the activity of keloid fibroblasts by activating the JAK/STAT signaling pathway.Heliyon · 2024Article
- Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid.International wound journal · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Keloid is a benign fibro-proliferative dermal tumour formed by an abnormal scarring response to injury and characterised by excessive collagen accumulation and invasive growth. The pathophysiology of keloids is complex, and the treatment for keloids is still an unmet medical need. Here, we investigated the transcriptional gene that influences keloid development by comparing keloid, non-lesioned keloid skin and normal skin as well as keloid fibroblast and normal fibroblast (GSE83286, GSE92566, GSE44270). Based on the analysis, 146 up-regulated genes and 48 down-regulated genes were found in keloid tissue compared with normal skin and keloid no-lesioned skin. Eleven genes were further identified by overlapping the DEGs from keloid tissue described previously with DEGs in keloid fibroblast. The overlapped genes included PRR16, SFRP2, EDIL3, GERM1, POSTN, PDE3A, GALNT5, F2RL2, EYA4, ZFHX4, and AIM2. POSTN is the most crucial node in PPI network, which mainly correlate to collagen-related genes. Moreover, siRNA knockdown identified POSTN is a crucial regulatory gene that regulates keloid fibroblast migration and collagen I, collagen III expression level. In conclusion, our study identified 11 hub genes that play crucial role in keloid formation and provided insights for POSTN to be the therapeutic target for keloid through bioinformatic analysis of three datasets. Additionally, our results would support the development of future therapeutic strategies.
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What OpenQuestion holds
Registered trials
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