MitoQ alleviates H₂O₂-induced mitochondrial dysfunction in keratinocytes through the Nrf2/PINK1 pathway

Area of Science:

• Dermatology
• Cell Biology
• Mitochondrial Medicine

Background:

• Oxidative stress is a key factor in vitiligo pathogenesis, damaging keratinocytes and disease progression.
• MitoQ, a mitochondria-targeted antioxidant, shows promise in preventing oxidative stress-related disorders.
• Downregulated expression of Nrf2, PINK1, Parkin, and LC3 is observed in vitiligo patients.

Purpose of the Study:

• To investigate the protective effects of MitoQ against oxidative stress in keratinocytes.
• To explore MitoQ's role in regulating key cellular pathways involved in oxidative damage.

Main Methods:

• HaCaT cells were treated with hydrogen peroxide (H2O2) and/or MitoQ.
• Nrf2, PINK1, and Parkin expression levels were analyzed.
• Mitophagy levels and Nrf2 nuclear translocation were assessed.
• Gene knockdown of NFE2L2 (Nrf2) or PINK1 was performed to evaluate pathway dependency.

Main Results:

• MitoQ mitigated H2O2-induced downregulation of Nrf2, PINK1, and Parkin.
• MitoQ reduced Nrf2 nuclear translocation and H2O2-induced mitophagy.
• Knockdown of NFE2L2 or PINK1 exacerbated oxidative stress, mitochondrial dysfunction, and cell death, conditions not alleviated by MitoQ.

Conclusions:

• MitoQ may protect against H2O2-induced mitochondrial oxidative stress by regulating the PINK1/Parkin pathway through Nrf2.
• These findings provide experimental evidence supporting MitoQ as a potential therapeutic agent for vitiligo.