ReviewClinical epigenetics2020
Epigenetic modification mechanisms involved in keloid: current status and prospect.
Review in Clinical epigenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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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
53 citing papers in PubMed, 85 citations in OpenAlex.
- Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).Molecular medicine reports · 2026Review
- Research advances in the pathogenesis and photodynamic therapy of pathological scars.Lasers in medical science · 2026Review
- Post-surgical electron beam radiotherapy for prevention of keloid recurrence: A retrospective study of 619 cases demonstrating low recurrence (6.5%) with optimised 18 Gy in two fractions.Clinical medicine (London, England) · 2026Article
- A Holistic Approach to Unravel Keloid Pathogenesis and Optimize Therapeutic Outcomes.Biomedicines · 2026Review
- Genetically Proxied Biological Aging and Risk of Hypertrophic Scar/Keloid-Coded Phenotypes: An Exploratory Two-Sample Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- The role of epigenetic modifications in cancer-associated fibroblasts.Frontiers in medicine · 2026Review
- Beyond blood pressure: the renin-angiotensin system as an innovative driver and therapeutic target in pathological scarring.Frontiers in pharmacology · 2026Review
- Epigenetic Landscapes in Ulcerative Colitis: From Mechanistic Insights to Clinical Translation.ACS omega · 2025Review
- Methylation of LINE-1 and Alu repetitive sequence in keloid.Scientific reports · 2025Article
- Salidroside Prevents Keloid Fibroblast Aggressive Progression by Upregulating miR-26a-5p to Inhibit JAG1.Cell biochemistry and biophysics · 2025Article
- FTO-mediated m6A demethylation of KLF4 promotes the proliferation and collagen deposition of keloid fibroblasts.Toxicology research · 2025Article
- MeCP2 promotes keloid progression by regulating ADAM12 expression and Wnt/β-catenin pathway.Archives of dermatological research · 2025Article
- IFNγ regulates ferroptosis in KFs by inhibiting the expression of SPOCD1 through DNMT3A.Cell death discovery · 2025Article
- Long non-coding RNAs promote colorectal cancer development through other epigenetic modifications.Gastroenterology report · 2025Review
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Association and mediation between circulating inflammatory proteins and skin fibrosis.Frontiers in endocrinology · 2025Article
- Update on the Pathogenesis of Keloid Formation.JID innovations : skin science from molecules to population health · 2024Review
- Unraveling the landscape of m6A RNA methylation in wound healing and scars.Cell death discovery · 2024Review
- Identification and Analysis of Immune Microenvironment-Related Genes for Keloid Risk Prediction and Their Effects on Keloid Proliferation and Migration.Biochemical genetics · 2024Article
- Targeting the nuclear long noncoding transcript LSP1P5 abrogates extracellular matrix deposition by trans-upregulating CEBPA in keloids.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloid, a common dermal fibroproliferative disorder, is benign skin tumors characterized by the aggressive fibroblasts proliferation and excessive accumulation of extracellular matrix. However, common therapeutic approaches of keloid have limited effectiveness, emphasizing the momentousness of developing innovative mechanisms and therapeutic strategies. Epigenetics, representing the potential link of complex interactions between genetics and external risk factors, is currently under intense scrutiny. Accumulating evidence has demonstrated that multiple diverse and reversible epigenetic modifications, represented by DNA methylation, histone modification, and non-coding RNAs (ncRNAs), play a critical role in gene regulation and downstream fibroblastic function in keloid. Importantly, abnormal epigenetic modification manipulates multiple behaviors of keloid-derived fibroblasts, which served as the main cellular components in keloid skin tissue, including proliferation, migration, apoptosis, and differentiation. Here, we have reviewed and summarized the present available clinical and experimental studies to deeply investigate the expression profiles and clarify the mechanisms of epigenetic modification in the progression of keloid, mainly including DNA methylation, histone modification, and ncRNAs (miRNA, lncRNA, and circRNA). Besides, we also provide the challenges and future perspectives associated with epigenetics modification in keloid. Deciphering the complicated epigenetic modification in keloid is hopeful to bring novel insights into the pathogenesis etiology and diagnostic/therapeutic targets in keloid, laying a foundation for optimal keloid ending.
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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 Socratic graph.