SynthesisNature communications2025
Multi-ancestry meta-analysis of keloids uncovers novel susceptibility loci in diverse populations.
Synthesis in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Distinct Molecular Signature of Earlobe Keloids: Integrated Transcriptomic Analysis of Extracellualr Matrix, Metalloproteinase, and Metabolic Pathways.Aesthetic plastic surgery · 2026Article
- Ancestry-linked IL-10 signaling and macrophage activation modulate fibroblast responses to oxidative stress in a PEG-based microphysiological system.npj biomedical innovations · 2026Article
- Clinical and Therapeutic Predictors of Keloid Recurrence: Outcomes in a European Cohort of 206 Patients.Journal of clinical medicine · 2026Article
- Endothelial system dysregulation underlies keloid development and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- A Comprehensive Review of Predictive Precision in Scar Medicine: From Molecular Predictors to Machine Learning Models.Clinical, cosmetic and investigational dermatology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Keloids are raised scars that grow beyond original wound boundaries, resulting in pain and disfigurement. Reasons for keloid development are not well-understood, and current treatment options are limited. Keloids are more likely to occur in darker-skinned individuals of African and Asian descent than in Europeans. We performed a genome-wide association study (GWAS) examining keloid risk across and within continental ancestry groups, incorporating 7837 cases and 1,593,009 controls. We detected 26 loci in the multi-ancestry analysis, 12 of which replicated in an independent dataset. Heritability estimates were 6%, 21%, and 34% for the European, East Asian, and African ancestry analyses, respectively. Genetically predicted gene expression and colocalization analyses identified 27 gene-tissue pairs, nine in skin and fibroblasts. Pathway analyses implicated integrin signaling and upstream regulators involved in cancer, fibrosis, and sex hormone signaling. This investigation nearly quintuples the number of keloid-associated risk loci, illuminating biological processes in keloid pathology.
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Registered trials
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