摘要

Skin photoaging, the most common skin damage, is caused by chronic UV irradiation. It is involved in the reduction, aging and apoptosis of fibroblasts (FBs) as well as the blockage of transforming growth factor-beta (TGF-beta)/Smad and p38 mitogen-actived protein kinase (MAPK) signaling pathways. Dermal multipotent stem cells (dMSCs) are a population of adult stem cells derived from dermis in recent years. It has been confirmed that dMSCs can activate or differentiate into FBs to participate in wound healing by producing and expressing TGF-beta and other cytokines. Considering the mechanism of skin photoaging and the role of dMSCs, we hold a hypothesis that dMSCs may be applied in skin photoaging by activating TGF-beta/Smad and p38 MAPK signaling pathways, and then stimulating FBs to secrete and synthesize collagen or elastin, heightening the extracellular matrix, finally eliminating wrinkles and strengthening skin elasticity. These would provide a novel approach for anti-skin photoaging.

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