Abstract
Human skin is submitted to hyperpigmentation disorders during our life: senile lentigo, linked to intrinsic ageing, leads to a loss of melanogenesis’ control while solar lentigo, linked to UV exposure, promotes an increase of oxidized proteins, melanogenesis and lipofuscin accumulation. SDF1 (Stromal cell-derived factor 1) was recently identified as key regulator of pigmentation via the inhibition of cAMP pathway in melanocytes. SDF1 expression is reduced in senescent fibroblasts during senile lentigo, pushing this protein as a strategic target for skin hyperpigmentation.
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