ArticleJPRAS open2019
Keloid pathophysiology: fibroblast or inflammatory disorders?
Article in JPRAS open, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Intralesional 5-Fluorouracil for Keloids: A Systematic Review.Journal of cutaneous medicine and surgeryPooled it
- Trial
- Phosphoglucose isomerase directs the inflammatory response, calcium influx and fibroblast migration in keloids.Future science OA · 2026Article
- Understanding and Comparing Current Practice for Ear Keloid Scars: A Narrative Systematic Review.Journal of plastic and reconstructive surgery · 2026Review
- Efficacy of peri-operative high-dose-rate interstitial brachytherapy in keloids: Can we scare the bad scar?Journal of contemporary brachytherapy · 2026Article
- Assessment of keloids recurrence rate in patients treated by brachytherapy versus electron beam radiotherapy versus surgical excision.JPRAS open · 2026Article
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- Fibroblast-Targeted Nanodelivery Systems: Mechanisms of Collagen Remodeling Regulation and Novel Strategies for Scar Repair.Pharmaceutics · 2026Review
- Xenium spatial transcriptomics identifies mesenchymal fibroblast expansion and conserved fibrotic ECM programs in keloid.Burns & trauma · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Ideal Surgical Incision Lines Minimizing Tension: A Proposal Based on Observations of Hypertrophic Scars and Keloids.Plastic and reconstructive surgery. Global open · 2025Article
- Regulatory role of POSTN in keloid pathogenesis.Molecular medicine reports · 2025Article
- Description of clinical and histopathological characteristics of keloids in a sub-Saharan African population.Skin health and disease · 2025Article
- Identification of potential biomarkers and mechanisms for keloid disorder based on comprehensive bioinformatics analysis and machine learning algorithms.BMC medical genomics · 2025Article
- Fibromodulin selectively accelerates myofibroblast apoptosis in cutaneous wounds by enhancing interleukin 1β signaling.Nature communications · 2025Article
- ERG transcriptionally activates SFRP1 to promote apoptosis of keloid fibroblasts and inhibit epithelial-mesenchymal transition and fibrosis through the Wnt3a/β-catenin pathway.Archives of dermatological research · 2025Article
- Targeting the Epigenome Reduces Keloid Fibroblast Cell Proliferation, Migration, and Invasion.The Journal of investigative dermatology · 2025Article
- Unveiling the Link: The Potential Roles of Vitamin D in Keloid Pathophysiology.Experimental dermatology · 2025Review
- Comparative effectiveness of plant-derived compounds in keloid management: a review.Frontiers in pharmacology · 2025Review
- EDN1 and NTF3 in keloid pathogenesis: computational and experimental evidence as novel diagnostic biomarkers for fibrosis and inflammation.Frontiers in genetics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundKeloids are defined as a benign dermal fibroproliferative disorder with no malignant potential. They tend to occur following trivial trauma or any form of trauma in genetically predisposed individuals. Keloids are known to grow beyond the margins of the wound and are common in certain body parts. The pathophysiology of keloid remains unclear, and fibroblasts have been presumed to be the main cells involved in keloid formation. Understanding the mechanism(s) of keloid formation could be critical in the identification of novel therapeutic regimen for the treatment of the keloids.
objectiveTo review the pertinent literature and provide updated information on keloid pathophysiology. DATA SOURCE: A Medline PubMed literature search was performed for relevant publications.
resultsA total of 66 publications were retrieved, with relevant publications on the etiology and pathogenesis as well as experimental studies on keloids. All articles were critically analyzed, and all the findings were edited and summarized.
conclusionThere is still no consensus as on what is the main driving cell to keloid formation. One may, however, hypothesize that keloid formation could be a result of an abnormal response to tissue injury, hence resulting in an exaggerated inflammatory state characterized by entry of excessive inflammatory cells into the wound, including macrophages, lymphocytes, and mast cells. These cells seem to release cytokines including transforming growth factor
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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.