ReviewPigment cell & melanoma research2020
The genetic architecture of vitiligo.
Review in Pigment cell & melanoma research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Second Guidelines for the Diagnosis and Treatment of Vitiligo in Japan (2025).The Journal of dermatology · 2026Guideline
- Review
- Vitiligo secondary to immunosuppressants: a pharmacovigilance study of the FDA Adverse Event Reporting System.Frontiers in immunology · 2026Article
- Genetics of Vitiligo: A Review.Clinical, cosmetic and investigational dermatology · 2026Review
- Gut and skin microbiome-metabolome pathways in vitiligo: from dysbiosis to immune activation and melanocyte dysfunction.Frontiers in immunology · 2026Review
- Dissecting age-specific genetic architecture of vitiligo through integrative Post-GWAS analysis.Frontiers in immunology · 2026Article
- Vitiligo.Nature reviews. Disease primers · 2025Review
- Familial Versus Non-Familial Vitiligo: Clinical Features, Anatomical Distribution, and Autoimmune Comorbidity from a Southern Taiwan Hospital.Medicina (Kaunas, Lithuania) · 2025Article
- Clinical patterns of vitiligo in Japan: A descriptive study using the JMDC claims database.The Journal of dermatology · 2025Article
- Inverse relationship between polygenic risk burden and age of onset of autoimmune vitiligo.American journal of human genetics · 2024Article
- Natural Sources of Therapeutic Agents Used in Skin Conditions.Life (Basel, Switzerland) · 2024Review
- Circadian clock gene expression and polymorphism in non-segmental vitiligo.Molecular biology reports · 2024Article
- Identification of Upregulating Genes, Transcription Factors, and miRNAs in Vitiligo. In silico Study.Clinical, cosmetic and investigational dermatology · 2024Article
- Disseminated Hypertrophic Discoid Lupus Erythematosus in a Patient with Vitiligo: A Case Report and Literature Review.Clinical, cosmetic and investigational dermatology · 2024Article
- Understanding of Pathomechanisms and Clinical Practice for Vitiligo.Annals of dermatology · 2023Review
- Vitiligo and insulin resistance as a component of metabolic syndrome: an analysis.Postepy dermatologii i alergologii · 2023Review
- Evidence for Epistatic Interaction betweenCells · 2023Article
- Melanocyte-keratinocyte cross-talk in vitiligo.Frontiers in medicine · 2023Review
- Article
- Occludin Promotes Adhesion of CD8Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Vitiligo is an autoimmune disease in which destruction of skin melanocytes results in patches of white skin and hair. Genome-wide linkage studies and genome-wide association studies in European ancestry cases identified over 50 vitiligo susceptibility loci, defining a model of melanocyte-directed autoimmunity. Vitiligo heritability is exceedingly high, ~2/3 coming from common and ~1/3 from rare genomic variants; ~20% of vitiligo risk is environmental. Vitiligo genetic risk is polygenic, with greater additive risk in multiplex vitiligo families than simplex cases. Vitiligo age-of-onset is bimodal, also involving a major genetic component; a MHC enhancer haplotype confers extreme risk for vitiligo (OR 8.1) and early disease onset, increasing expression of HLA-DQB1 mRNA and HLA-DQ protein and thus perhaps facilitating presentation of triggering antigens. Vitiligo triggering also involves a major environmental component; dramatic delay in vitiligo age-of-onset, especially from 1973 to 2004, suggests that exposure or response to a key vitiligo environmental trigger diminished during this period. Together, these findings provide deep understanding of vitiligo pathogenesis and genetic architecture, suggesting that vitiligo represents a tractable model for investigating complex disease genetic architecture and predictive aspects of personalized medicine.
Indexed as
Identifiers
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.