The Role of Oxidative Stress in Vitiligo: An Update on Its Pathogenesis and Therapeutic Implications

Vitiligo is an autoimmune skin disorder caused by dysfunctional pigment-producing melanocytes which are attacked by immune cells. Oxidative stress is considered to play a crucial role in activating consequent autoimmune responses related to vitiligo. Melanin synthesis by melanocytes is the main intr...

Full description

Saved in:
Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2023-03, Vol.12 (6), p.936
Main Authors: Chang, Wei-Ling, Ko, Chi-Hsiang
Format: Article
Language:English
Subjects:
Adaptive immunity
Antigens
Antioxidants
Antioxidants - metabolism
Antioxidants - therapeutic use
autoantigen
autoimmune skin disorder
Autoimmunity
Care and treatment
Cytotoxicity
Development and progression
Enzymes
Health aspects
Humans
Hypopigmentation
Immune response
Inflammation
Kinases
Melanin
melanocyte
Melanocytes
Metabolism
Oxidation
Oxidative stress
Oxidative Stress - physiology
Pathogenesis
Patients
Proteins
Reactive oxygen species
reactive oxygen species (ROS)
Reactive Oxygen Species - metabolism
Review
Skin
Skin diseases
Transcription factors
Tumor necrosis factor-TNF
Vitiligo
Vitiligo - drug therapy
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Vitiligo is an autoimmune skin disorder caused by dysfunctional pigment-producing melanocytes which are attacked by immune cells. Oxidative stress is considered to play a crucial role in activating consequent autoimmune responses related to vitiligo. Melanin synthesis by melanocytes is the main intracellular stressor, producing reactive oxygen species (ROS). Under normal physiological conditions, the antioxidative nuclear factor erythroid 2-related factor 2 (Nrf2) pathway functions as a crucial mediator for cells to resist oxidative stress. In pathological situations, such as with antioxidant defects or under inflammation, ROS accumulate and cause cell damage. Herein, we summarize events at the cellular level under excessive ROS in vitiligo and highlight exposure to melanocyte-specific antigens that trigger immune responses. Such responses lead to functional impairment and the death of melanocytes, which sequentially increase melanocyte cytotoxicity through both innate and adaptive immunity. This report provides new perspectives and advances our understanding of interrelationships between oxidative stress and autoimmunity in the pathogenesis of vitiligo. We describe progress with targeted antioxidant therapy, with the aim of providing potential therapeutic approaches.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells12060936