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. 2024 Feb 25;20(5):1778–1795. doi: 10.7150/ijbs.92897

Table 1.

The mechanisms of exosomes in vitiligo pathogenesis

Exosome Source Model Mechanism Ref.
Blood of segmental vitiligo patients Human primary keratinocytes and melanocytes MiR-493-3p-overexpressing keratinocyte induced melanocyte apoptosis and decreased melanin synthesis through miR-493-3p/HNRNPU/COMT/dopamine axis (46)
Peripheral blood of vitiligo patients Human melanocytes cell Circulating exosomes inhibited melanin content, tyrosinase activity, and melanogenesis-related protein expression via transferring miR-21-5p and inhibiting SATB1 expression (47)
Serum of progressive vitiligo patients Progressive vitiligo patients Hsa-miR-487b-3p was significantly lower and positively correlated with the area of lesions (14)
Keratinocytes in vitiligo lesions NHEM MiR‐200c up-regulated the expression of melanogenesis‐related genes via inhibiting SOX1 and activating β‐catenin (48)