Autophagy is a membrane traffic system that provides sustainable degradation of cellular components for homeostasis, and is thus considered to promote health and longevity, though its activity declines with aging. The present findings show deterioration of autophagy in association with premature skin aging. Autophagy flux was successfully determined in skin tissues, which demonstrated significantly decreased autophagy in hyperpigmented skin such as that seen in senile lentigo. Furthermore, an exacerbated decline in autophagy was confirmed in xerotic hyperpigmentation areas, accompanied by severe dehydration and a barrier defect, which showed correlations with skin physiological conditions. The enhancement of autophagy in skin ex vivo ameliorated skin integrity, including pigmentation and epidermal differentiation. The present results indicate that the restoration of autophagy can contribute to improving premature skin aging by various intrinsic and extrinsic factors via the normalization of protein homeostasis.

Background/Objectives: Temporary decreases in dermal collagen caused by artificial ultraviolet exposure are largely affected by increased epidermis-derived matrix metalloproteinase (MMP)-1 levels. However, the role of epidermal MMP-1 in dermal tissue remodeling induced by chronic sun exposure remains unclear. This study aimed to clarify the involvement of epidermal and dermal MMP-1 in dermal collagen reduction induced by chronic sun exposure. Methods: Immunofluorescent staining of 30 facial skin tissue samples was performed to visualize MMP-1. The fluorescence intensity of epidermal MMP-1 observed on microscopic images was analyzed in relation to the severity of dermal tissue remodeling and the dermal collagen fiber density. A similar correlation analysis of the number of dermal MMP-1-positive cells was also performed. Results: Epidermal MMP-1 was observed in the stratum spinosum of skin without severe tissue remodeling; however, in skin with severe dermal tissue remodeling, MMP-1 was localized throughout the epidermis. The epidermal MMP-1 signal area and dermal collagen fiber density were negatively correlated (ρ = −0.383; p = 0.0002; n = 90). However, the ratio of dermal MMP-1-positive cells to total dermal cells was only negatively correlated with the collagen fiber density in skin that was not severely remodeled (ρ = −0.746; p = 0.001; n = 15). Conclusions: Epidermal MMP-1 is involved in the tissue remodeling of skin that is subjected to chronic sun exposure and short-term ultraviolet radiation exposure. However, dermal-cell-derived MMP-1 may be involved in biological processes that require an immediate collagen degradation response. The results of this study demonstrate the importance of controlling epidermal MMP-1 to inhibit dermal tissue remodeling induced by chronic sun exposure and provide new insights that are beneficial to the development of anti-photoaging skincare cosmetics.