ArticleExperimental dermatology2017
The nuclear factor (erythroid-derived 2)-like 2 (NRF2) antioxidant response promotes melanocyte viability and reduces toxicity of the vitiligo-inducing phenol monobenzone.
Article in Experimental dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Vitiligo as a Failure of Immune Resolution and Tissue Regeneration: From Stress Signals to Targeted Immune Modulation.Clinical reviews in allergy & immunology · 2026Review
- Modulation of Inflammatory and Apoptotic Pathways by Tamarix Aphylla Essential Oil in TNBS-Induced Colitis: A Focus on Cytokine Balancing, NF-κB, p38 MAPK, and Nrf2 Activation.Applied biochemistry and biotechnology · 2026Article
- Oxidative stress in refractory and recurrent vitiligo: from immune amplification mechanisms to potential stratified antioxidant combination therapy.Frontiers in immunology · 2026Review
- Cullin-3 and Regulatory Biomolecules Profiling in Vitiligo: Integrated Docking, Clinical, and In Silico Insights.Biomolecules · 2025Article
- Predictive analysis of vitiligo treatment drugs using degree and neighborhood degree-based topological descriptors.Scientific reports · 2025Article
- A Cell-Based Evaluation of the Tyrosinase-Mediated Metabolic Activation of Leukoderma-Inducing Phenols, II: The Depletion ofBiomolecules · 2025Article
- Post-translational modification in the pathogenesis of vitiligo.Immunologic research · 2024Review
- Mechanisms of action ofPharmaceutical biology · 2023Article
- NRF2 in the Epidermal Pigmentary System.Biomolecules · 2022Review
- Current Concepts of Vitiligo Immunopathogenesis.Biomedicines · 2022Review
- Research Progress on Targeted Antioxidant Therapy and Vitiligo.Oxidative medicine and cellular longevity · 2022Review
- Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging.International journal of molecular sciences · 2021Review
- Vitiligo and Melanoma-Associated Vitiligo: Understanding Their Similarities and Differences.American journal of clinical dermatology · 2020Review
- The convergence theory for vitiligo: A reappraisal.Experimental dermatology · 2019Review
- RNA-seq Reveals Dysregulation of Novel Melanocyte Genes upon Oxidative Stress: Implications in Vitiligo Pathogenesis.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Vitiligo, characterised by progressive melanocyte death, can be initiated by exposure to vitiligo-inducing phenols (VIPs). VIPs generate oxidative stress in melanocytes and activate the master antioxidant regulator NRF2. While NRF2-regulated antioxidants are reported to protect melanocytes from oxidative stress, the role of NRF2 in the melanocyte response to monobenzone, a clinically relevant VIP, has not been characterised. We hypothesised that activation of NRF2 may protect melanocytes from monobenzone-induced toxicity. We observed that knockdown of NRF2 or NRF2-regulated antioxidants NQO1 and PRDX6 reduced melanocyte viability, but not viability of keratinocytes and fibroblasts, suggesting that melanocytes were preferentially dependent upon NRF2 activity for growth compared to other cutaneous cells. Furthermore, melanocytes activated the NRF2 response following monobenzone exposure and constitutive NRF2 activation reduced monobenzone toxicity, supporting NRF2's role in the melanocyte stress response. In contrast, melanocytes from individuals with vitiligo (vitiligo melanocytes) did not activate the NRF2 response as efficiently. Dimethyl fumarate-mediated NRF2 activation protected normal and vitiligo melanocytes against monobenzone-induced toxicity. Given the contribution of oxidant-antioxidant imbalance in vitiligo, modulation of this pathway may be of therapeutic interest.
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