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Targeting Oxidative Stress to Treat Vitiligo: Clinical and Molecular Evidence
Noemi Aprile1, Simona Scano2, Barbara Bellei2
1UOSVD Dermatology and Allergology, Hospital Vito Fazzi, 73100 Lecce, Italy.
Abstract:
Vitiligo is a chronic autoimmune disease characterized by the destruction of epidermal melanocyte, resulting in well-demarcated white patches on the skin. Despite the established use of corticosteroids and calcineurin inhibitors and the recent introduction of Janus kinase (JAK) inhibitors, a breakthrough targeted therapy that interrupts the IFN-γ signaling pathway, stable repigmentation remains a major clinical challenge, necessitating deeper investigation into its pathogenesis. Among the factors contributing to vitiligo, including genetic predisposition and autoimmunity, oxidative stress is a central driver of melanocyte damage and the subsequent autoimmune response. Chronic oxidative disequilibrium (high ROS level and impaired mitochondrial activity) and reduced antioxidant capacity (Nrf2/ARE pathway and catalase deficiency) function as triggering factors upstream of most other pathogenic pathways. Consequently, targeting oxidative stress, either as a monotherapy or in synergy with emerging targeted treatments, remains a pivotal area of therapeutic interest even in the current era of targeted therapies. Still, a significant gap remains the lack of standardized oxidative biomarkers to monitor disease activity and therapeutic response. Identifying these indicators is essential for personalized clinical management in vitiligo. This review examines how chronic oxidative disequilibrium and a reduced antioxidant capacity initiate and sustain the autoimmune cascade, leading to disease onset and progression.
Insights
Vitiligo pathogenesis involves oxidative stress damaging melanocytes. Targeting this imbalance and identifying biomarkers are crucial for effective treatment and managing this chronic autoimmune skin condition.
Area of Science:
- Dermatology
- Immunology
- Biochemistry
Background:
- Vitiligo is a chronic autoimmune disease causing melanocyte destruction and skin depigmentation.
- Current treatments like corticosteroids, calcineurin inhibitors, and JAK inhibitors show limitations in achieving stable repigmentation.
- Understanding vitiligo pathogenesis is crucial for developing advanced therapies.
Purpose of the Study:
- To review the role of oxidative stress in vitiligo pathogenesis.
- To explore the link between oxidative disequilibrium, reduced antioxidant capacity, and autoimmune responses in vitiligo.
- To highlight the need for oxidative biomarkers in clinical management.
Main Methods:
- Literature review focusing on the role of oxidative stress in vitiligo.
- Analysis of the interplay between genetic predisposition, autoimmunity, and oxidative damage.
- Examination of the Nrf2/ARE pathway and catalase in antioxidant defense.
Main Results:
- Oxidative stress, characterized by high reactive oxygen species (ROS) and impaired mitochondrial activity, is a central driver of melanocyte damage.
- Reduced antioxidant capacity, including deficiencies in the Nrf2/ARE pathway and catalase, exacerbates oxidative disequilibrium.
- These factors initiate and sustain the autoimmune cascade, contributing to vitiligo onset and progression.
Conclusions:
- Targeting oxidative stress is a key therapeutic strategy, potentially synergistic with existing and emerging treatments.
- Development of standardized oxidative biomarkers is essential for monitoring disease activity and treatment response.
- Personalized clinical management of vitiligo requires a deeper understanding of oxidative stress mechanisms.
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