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implies that combining therapies that reverse defects in keratinocytes metabolism with JAK inhibitors could be a novel approach to treating vitiligo ( Nrf2-ARE pathway In vitiligo, inactive Nrf2 signaling is ineffective in protecting HEM from H 2 O 2 -induced OS damage and, therefore, rarely prevents melanocyte apoptosis by mediating its downstream antioxidant gene heme oxygenase-1 (HO-1) (120)

Mesenchymal stem cell-derived exosomes overexpressing SRC-3 protect mice from cerebral ischemia by inhibiting ferroptosis

GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild-type mice and changes the transcriptional response of reactive glia in mouse model for Alzheimers disease

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