ArticleAnnals of dermatology2012
Role of keratinocytes in the development of vitiligo.
Article in Annals of dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed.
- Mechanistic Insights into Phytocompounds for Vitiligo Therapy: Current Evidence and Future Opportunities.Antioxidants (Basel, Switzerland) · 2026Review
- Neuropeptide Y drives vitiligo progression via NPYR-mediated NF-κB activation: a novel therapeutic target.Scientific reports · 2026Article
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Non-coding RNAs (miRNAs - circRNAs - lncRNAs) and genes interact with the regulation of vitiligo.Archives of dermatological research · 2025Article
- 308-nm excimer laser combined with piperine promotes melanin synthesis through PTEN/PDK1/GSK3b regulation of keratinocyte paracrine.Archives of dermatological research · 2025Article
- The Treatment of Refractory Vitiligo With Autologous Cultured Epithelium Grafting: A Real-World Retrospective Cohort Study.Stem cells translational medicine · 2024Article
- Identification and validation of RNA-binding protein SLC3A2 regulates melanocyte ferroptosis in vitiligo by integrated analysis of single-cell and bulk RNA-sequencing.BMC genomics · 2024Article
- Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis.Clinical, cosmetic and investigational dermatology · 2024Review
- Human-Induced Pluripotent Stem Cell‒Derived Keratinocytes, as Therapeutic Option in Vitiligo.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Extraciliary OFD1 Is Involved in Melanocyte Survival through Cell Adhesion to ECM via Paxillin.International journal of molecular sciences · 2023Article
- Aquaporin-3 Downregulation in Vitiligo Keratinocytes Increases Oxidative Stress of Melanocytes.Biomolecules & therapeutics · 2023Article
- The Role of Oxidative Stress in Vitiligo: An Update on Its Pathogenesis and Therapeutic Implications.Cells · 2023Review
- Current Status of Cell-Based Therapies for Vitiligo.International journal of molecular sciences · 2023Review
- Melanocyte-keratinocyte cross-talk in vitiligo.Frontiers in medicine · 2023Review
- Cannabidiol Application Increases Cutaneous Aquaporin-3 and Exerts a Skin Moisturizing Effect.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Wound-Healing and Skin-Moisturizing Effects ofHealthcare (Basel, Switzerland) · 2021Article
- Mesenchymal Stem Cells Antagonize IFN-Induced Proinflammatory Changes and Growth Inhibition Effects via Wnt/β-Catenin and JAK/STAT Pathway in Human Outer Root Sheath Cells and Hair Follicles.International journal of molecular sciences · 2021Article
- Is vitiligo associated with systemic aquaporin-3 deficiency?Postepy dermatologii i alergologii · 2021Article
- Article
- Effect of Astaxanthin on the Expression and Activity of Aquaporin-3 in Skin in an In-Vitro Study.Life (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitiligo is an acquired depigmentary disorder of the skin that results from the loss of functioning epidermal melanocytes. Most studies on vitiligo have concentrated on the abnormality of melanocytes rather than the abnormality of keratinocytes; however, epidermal melanocytes form a functional and structural unit with neighboring keratinocytes. In fact, direct cell-to cell contact stimulates in vitro proliferation of melanocytes, and growth factors produced by adjacent keratinocytes regulate the proliferation and differentiation of melanocytes. The potential role of keratinocyte-derived cytokines has also been presented. We focused on the structural changes in vitiliginous keratinocytes, which may result in loss of melanocytes, to examine the pathomechanism of vitiligo. The results of a comparison between depigmented and normally pigmented epidermis in patients with vitiligo showed that the keratinocytes in the depigmented epidermis were more vulnerable to apoptosis. Impaired Phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase (Akt) activation followed by reduced nuclear factor-κB activation under increased tumor necrosis factor-α levels was demonstrated as a mechanism for keratinocyte apoptosis. The role of aquaporin 3 in keratinocyte apoptosis was addressed based on the relationship between the PI3K/AKT pathway and the E-cadherin-catenin complex. Apoptotic keratinocytes induced a lower expression of keratinocyte-derived factors, including stem cell factor, in depigmented epidermis, resulting in passive melanocyte death.
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Registered trials
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