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This poor differentiation may be explained by the increased activity of the NOTCH signaling pathway, a key regulator of stem cell fate and self-renewal, and by reduced stimulation of the non-canonical Wnt pathway, which modulates cell polarity, migration, and lineage commitment under hypoxic conditions [106,153]

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This was evidenced in mouse models of chemotherapy-induced POF, where estrogen-sensitive ovarian epithelial (OSE)-like cells derived from human-induced pluripotent stem cells were transplanted into damaged ovaries

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