ArticleThe Journal of investigative dermatology2015
Altered E-Cadherin Levels and Distribution in Melanocytes Precede Clinical Manifestations of Vitiligo.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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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
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 149 citations in OpenAlex.
- Second Guidelines for the Diagnosis and Treatment of Vitiligo in Japan (2025).The Journal of dermatology · 2026Guideline
- Genome-wide association meta-analyses combining multiple risk phenotypes provide insights into the genetic architecture of cutaneous melanoma susceptibility.Nature genetics · 2020Pooled it
- Topical application of simvastatin acid sodium salt and atorvastatin calcium salt in vitiligo patients. Results of the randomized, double-blind EVRAAS pilot study.Scientific reports · 2024Trial
- Personalized Approaches to Facial Vitiligo: A Comprehensive Review From Clinical Phenotypes to Novel Therapeutic Strategies.Annals of dermatology · 2026Review
- Repigmentation Competence in Vitiligo: Integrating Immune, Regulatory, Regenerative, and Microenvironmental Axes.Journal of personalized medicine · 2026Review
- Review
- Aberrant laminin signaling drives melanocyte dedifferentiation and unveils a tractable therapeutic target in vitiligo.Nature communications · 2026Article
- Atypical E-cadherin attachments mediate melanoblast migration through confined epithelial spaces.The Journal of cell biology · 2026Article
- Pathogenesis of Vitiligo: Integrating Immune and Non-Immune Cell Crosstalk.The Journal of dermatology · 2026Review
- Immune control of functional memory CD8 T cells in normal-appearing vitiligo skin.Science advances · 2025Article
- Vitiligo.Nature reviews. Disease primers · 2025Review
- Shared Immunopathogenic Mechanisms in Chronic Spontaneous Urticaria, Vitiligo, and Hashimoto's Thyroiditis: The Role of Oxidative Stress and Vitamin D.Life (Basel, Switzerland) · 2025Review
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Linking IFN-γ-Mediated Pathogenesis to ROCK-Targeted Therapy in a Scalable iPSCs-Based Vitiligo Model.International journal of molecular sciences · 2025Article
- Vitiligo.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025Review
- The immunological pathogenesis of vitiligo and the potential role of mesenchymal stromal/stem cells in its treatment.Journal of translational medicine · 2025Review
- Oxidative Stress and Skin Diseases: The Role of Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- [Vitiligo-update on pathogenesis, diagnostics and therapy].Dermatologie (Heidelberg, Germany) · 2025Review
- Paeoniflorin regulates RhoA/ROCK1 and Nrf2 pathways in PDLIM1-dependent or independent manners in oxidative stressed melanocytes.Archives of dermatological research · 2024Article
- Genomic insights into local adaptation and phenotypic diversity of Wenchang chickens.Poultry science · 2024Article
Corrections and comments
- Commented on byEcad vitiliGONE.2015
- Commented on by
Authors and funding
13 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitiligo is the most common depigmenting disorder resulting from the loss of melanocytes from the basal epidermal layer. The pathogenesis of the disease is likely multifactorial and involves autoimmune causes, as well as oxidative and mechanical stress. It is important to identify early events in vitiligo to clarify pathogenesis, improve diagnosis, and inform therapy. Here, we show that E-cadherin (Ecad), which mediates the adhesion between melanocytes and keratinocytes in the epidermis, is absent from or discontinuously distributed across melanocyte membranes of vitiligo patients long before clinical lesions appear. This abnormality is associated with the detachment of the melanocytes from the basal to the suprabasal layers in the epidermis. Using human epidermal reconstructed skin and mouse models with normal or defective Ecad expression in melanocytes, we demonstrated that Ecad is required for melanocyte adhesiveness to the basal layer under oxidative and mechanical stress, establishing a link between silent/preclinical, cell-autonomous defects in vitiligo melanocytes and known environmental stressors accelerating disease expression. Our results implicate a primary predisposing skin defect affecting melanocyte adhesiveness that, under stress conditions, leads to disappearance of melanocytes and clinical vitiligo. Melanocyte adhesiveness is thus a potential target for therapy aiming at disease stabilization.
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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.