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When activated by stress-induced hormonal imbalances, these pathways promote the production of pro-inflammatory cytokines and genes associated with oxidative stress, increasing the overall oxidative burden on cells (53)
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Furthermore, MMP-9 is elevated in the skin and plasma of patients with common vitiligo, being produced in keratinocytes by the stimulation of TNFα and IFNγ and associated with E-cadherin cleavage.44 The DKK1 protein, which reduces melanogenesis and certain somatic functions of melanocytes, is overexpressed by lesional fibroblasts in vitiligo.45 Similarly, there is a greater expression of fibronectin, a key protein in intercellular communication by binding to integrins, in the dermis of patients with vitiligo compared with healthy controls.43 Additionally, elastin is reduced in lesional dermis, but collagen fibers show no difference when compared to unaffected skin.46 Oxidative changes Cutaneous melanocytes, located in the organ with the greatest interface with the external environment and, consequently, the most exposed to ultraviolet radiation and pollutants, are particularly vulnerable to excessive production of reactive oxygen species (ROS)
