ReviewCold Spring Harbor perspectives in biology2023
Keloid Disorder: Genetic Basis, Gene Expression Profiles, and Immunological Modulation of the Fibrotic Processes in the Skin.
Review in Cold Spring Harbor perspectives in biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 40 citations in OpenAlex.
- Distinct Molecular Signature of Earlobe Keloids: Integrated Transcriptomic Analysis of Extracellualr Matrix, Metalloproteinase, and Metabolic Pathways.Aesthetic plastic surgery · 2026Article
- LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.Lasers in surgery and medicine · 2026Article
- The OX40-OX40L Co-Stimulatory Pathway as a Shared Driver of Immune Persistence in Skin and Airway Inflammation.Clinical reviews in allergy & immunology · 2026Review
- POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).Molecular medicine reports · 2026Review
- Metabolic reprogramming and ferroptosis in keloid pathogenesis: new insights for targeted therapy.Molecular biology reports · 2026Review
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- Lipid droplet-mediated macrophage reprogramming drives fibroblast activation in keloid-associated inflammation.Cell communication and signaling : CCS · 2026Article
- LncRNA RNF144A-AS1 increases P300-mediated H4K5 acetylation of PDE4 to promote keloid fibrosis.Biomedical engineering online · 2026Article
- Potential Causal Association Between Plasma Lipidomes and Keloid: Analysis from a Two-Sample Mendelian Randomization.Clinical, cosmetic and investigational dermatology · 2026Article
- Identification of potential biomarkers related to mannose metabolism in keloids: analysis of integrated bulk RNA-seq and scRNA-seq.Frontiers in immunology · 2026Article
- A Nomogram Predicting Decreased Quality of Life in Patients with Keloids.Clinical, cosmetic and investigational dermatology · 2026Article
- BMP2-induced Adam12International journal of biological sciences · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Predicting corticosteroid resistance and recurrence in keloids: a machine learning study integrating dermatoscopy and ultrasound.Frontiers in medicine · 2026Article
- Identification and Preliminary mRNA Validation of Key Genes Associated with Tolerogenic Dendritic Cells in Keloid Based on Transcriptome Data.Clinical, cosmetic and investigational dermatology · 2026Article
- Fibroblast Dynamics in Keloid Pathogenesis: Unraveling Cellular Crosstalk and Novel Therapeutic Targets.Dermatology research and practice · 2026Review
- Regulatory role of POSTN in keloid pathogenesis.Molecular medicine reports · 2025Article
- Retrospective study comparing three approaches for keloids: surgery + radiotherapy, surgery + pharmacological injection, and surgery alone.BMC surgery · 2025Observational
- Association between keloid and mental disorders: perspective from genetic evidence.Annals of general psychiatry · 2025Article
- Hypertrophic and Keloid Scar Management: Advances in Diagnosis, Perioperative Care, and Anesthetic Modulation.Cureus · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Keloid disorder, a group of fibroproliferative skin disorders, is clinically comprised of keloids, hypertrophic scars, keloidalis nuchae, and acne keloidalis. The prototype of these disorders is keloids, which manifest as cutaneous lesions with excessive deposition of collagen following an initiating trauma of varying degrees. The principal cell type responsible for collagen accumulation is the myofibroblast, and its gene expression is modulated by a network of regulatory factors, including cytokines, growth factors, and noncoding RNA species. In addition, keloids harbor a number of inflammatory cells, including macrophages and mast cells, that interact with fibroblastic cells by direct contact or by paracrine actions. Transforming growth factor-β1/Smad signaling regulates the expression of genes encoding extracellular matrix proteins and also controls cell proliferation and apoptosis. A key profibrotic molecule is the fibronectin splice variant cellular fibronectin extracellular domain A (cFN-EDA), which interacts with a number of cell-surface integrins and TLR4, contributing to the modulation of gene expression by lesional fibroblasts. Collectively, these complex cellular interactions result in accumulation of collagen with clinical development and growth of keloid lesions. Understanding of the precise pathomechanistic details of keloid formation will provide targets for pharmacological interference toward treatment of the keloid disorder, a group of currently difficult to treat skin diseases.
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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 OpenQuestion graph.