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Besides the increase in melanin content, AL lesions are characterized by epidermal alterations such as proliferation/differentiation disbalance or mitochondrial dysfunction, dermal photoaging marks, and disorganization of the dermal extracellular matrix (ECM) [21,22,23]. In particular, AL lesions present an impairment of the cutaneous structure with a marked elongation of the dermalepidermal junction (DEJ), an accumulation of melanin in the epidermis, especially in the rete ridges [21]

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