ArticleDisease markers2015
Genome-Wide Scan for Methylation Profiles in Keloids.
Article in Disease markers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Epidemiology of keloids among university students in Uganda.Dermatology reports · 2026Article
- Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).Molecular medicine reports · 2026Review
- The Causal Role of Uterine Fibroid in Keloid and Hypertrophic Scar: A Bidirectional Mendelian Randomization Study on European Populations.Current pharmaceutical biotechnology · 2025Article
- Update on the Pathogenesis of Keloid Formation.JID innovations : skin science from molecules to population health · 2024Review
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- Multi-omics integrative analysis reveals the role of tumor necrosis factor superfamily member 4 in keloidal scarring.American journal of translational research · 2023Article
- An updated review of the immunological mechanisms of keloid scars.Frontiers in immunology · 2023Review
- Epigenetic Dysregulation in Autoimmune and Inflammatory Skin Diseases.Clinical reviews in allergy & immunology · 2022Review
- The Emerging Therapeutic Targets for Scar Management: Genetic and Epigenetic Landscapes.Skin pharmacology and physiology · 2022Review
- Advances in the pathogenesis and clinical application prospects of tumor biomolecules in keloid.Burns & trauma · 2022Review
- OMICS Approaches Evaluating Keloid and Hypertrophic Scars.International journal of inflammation · 2022Review
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- Epigenetic regulation of cellular functions in wound healing.Experimental dermatology · 2021Review
- Epigenetic modification mechanisms involved in keloid: current status and prospect.Clinical epigenetics · 2020Review
- Identification of Differentially Methylated CpG Sites in Fibroblasts from Keloid Scars.Biomedicines · 2020Article
- The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing.Biomedicines · 2020Review
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- Understanding Keloid Pathobiology From a Quasi-Neoplastic Perspective: Less of a Scar and More of a Chronic Inflammatory Disease With Cancer-Like Tendencies.Frontiers in immunology · 2019Review
- Methylation of secreted frizzled-related protein 1 (SFRP1) promoter downregulates Wnt/β-catenin activity in keloids.Journal of molecular histology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are benign fibroproliferative tumors of the skin which commonly occur after injury mainly in darker skinned patients. Medical treatment is fraught with high recurrence rates mainly because of an incomplete understanding of the biological mechanisms that lead to keloids. The purpose of this project was to examine keloid pathogenesis from the epigenome perspective of DNA methylation. Genome-wide profiling used the Infinium HumanMethylation450 BeadChip to interrogate DNA from 6 fresh keloid and 6 normal skin samples from 12 anonymous donors. A 3-tiered approach was used to call out genes most differentially methylated between keloid and normal. When compared to normal, of the 685 differentially methylated CpGs at Tier 3, 510 were hypomethylated and 175 were hypermethylated with 190 CpGs in promoter and 495 in nonpromoter regions. The 190 promoter region CpGs corresponded to 152 genes: 96 (63%) were hypomethylated and 56 (37%) hypermethylated. This exploratory genome-wide scan of the keloid methylome highlights a predominance of hypomethylated genomic landscapes, favoring nonpromoter regions. DNA methylation, as an additional mechanism for gene regulation in keloid pathogenesis, holds potential for novel treatments that reverse deleterious epigenetic changes. As an alternative mechanism for regulating genes, epigenetics may explain why gene mutations alone do not provide definitive mechanisms for keloid formation.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.