ArticlePLoS genetics2022
Combined analyses of RNA-sequence and Hi-C along with GWAS loci-A novel approach to dissect keloid disorder genetic mechanism.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Distinct Molecular Signature of Earlobe Keloids: Integrated Transcriptomic Analysis of Extracellualr Matrix, Metalloproteinase, and Metabolic Pathways.Aesthetic plastic surgery · 2026Article
- A Holistic Approach to Unravel Keloid Pathogenesis and Optimize Therapeutic Outcomes.Biomedicines · 2026Review
- Effects of exosomes from human dental pulp stem cells on the biological behavior of human fibroblasts.Scientific reports · 2025Article
- Identifying core genes in keloid and investigating immune infiltration and pan-cancer associations using eQTL and machine learning.Bioinformatics advances · 2025Article
- Susceptibility ofHeliyon · 2024Article
- Cellular and Molecular Processes in Wound Healing.Biomedicines · 2023Review
- MicroRNA-182-5p Inhibits Hypertrophic Scar Formation by Inhibiting the Proliferation and Migration of Fibroblasts via SMAD4 Pathway.Clinical, cosmetic and investigational dermatology · 2023Article
- Revisiting Spontaneous Keloids: Aetiology, Genetics and Evidence for a Polygenic Pathogenesis.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloid disorder is a tumour-like disease with invasive growth and a high recurrence rate. Genetic contribution is well expected due to the presence of autosomal dominant inheritance and various genetic mutations in keloid lesions. However, GWAS failed to reveal functional variants in exon regions but single nucleotide polymorphisms in the non-coding regions, suggesting the necessity of innovative genetic investigation. This study employed combined GWAS, RNA-sequence and Hi-C analyses to dissect keloid disorder genetic mechanisms using paired keloid tissues and normal skins. Differentially expressed genes, miRNAs and lncRNAs mined by RNA-sequence were identified to construct a network. From which, 8 significant pathways involved in keloid disorder pathogenesis were enriched and 6 of them were verified. Furthermore, topologically associated domains at susceptible loci were located via the Hi-C database and ten differentially expressed RNAs were identified. Among them, the functions of six molecules for cell proliferation, cell cycle and apoptosis were particularly examined and confirmed by overexpressing and knocking-down assays. This study firstly revealed unknown key biomarkers and pathways in keloid lesions using RNA-sequence and previously reported mutation loci, indicating a feasible approach to reveal the genetic contribution to keloid disorder and possibly to other diseases that are failed by GWAS analysis alone.
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Registered trials
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