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Microplastics and Skin Aging: Disruption of Barrier Function and Induction of Fibroblast Senescence

Experimental Dermatology 2024 7 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 55 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Yujie Ouyang, Yujie Ouyang, Songjiang Wu, Yuanyuan Zhao, Yibo Hu, Ling Jiang, Li Lei, Chuhan Fu, Li Lei, Li Lei, Yushan Zhang, Xiaolei Duan, Jinhua Huang, Jing Chen, Qinghai Zeng

Summary

Researchers investigated how polystyrene microplastics affect skin health using lab-grown skin cells and gene expression analysis. They found that microplastic exposure disrupted the skin's protective barrier by inhibiting normal skin cell development and accelerated aging in the deeper skin layer by triggering cellular senescence. The study suggests that microplastics may contribute to premature skin aging and weakened skin barrier function, adding to the growing understanding of how these particles affect human health.

Polymers
Body Systems
Study Type In vitro

ABSTRACT Microplastics (MPs) have emerged as a major concern among contemporary pollutants, but there is still limited knowledge regarding their impact on skin function. To address this issue, we conducted a transcriptome analysis on skin tissue that had been exposed to polystyrene (PS), which is one of the most prevalent type of MPs that can be absorbed through the skin. The results of our study, obtained through functional enrichment analysis and the experiment of treating HaCaT with PS, revealed that PS may have an effect on skin barrier function, specifically the permeability barrier through inhibiting keratinocyte differentiation. Additionally, PS also induced dysfunction in the extracellular matrix (ECM). Mechanistically, we observed that PS induced fibroblasts senescence and increased the secretion of senescence‐related characteristics. Furthermore, the expression of core genes related to the ECM, such as COL1A1 , COL1A2 and SPP1 , was found to be down‐regulated in PS‐treated fibroblasts. Moreover, an in vitro experiment provided evidence of the involvement of PPARγ in PS‐induced fibroblast senescence. In conclusion, our study has identified PS as a causal factor for skin barrier dysfunction. Additionally, PS induces fibroblast senescence, leading to ECM dysfunction and contributing to skin aging. These findings further strengthen the understanding and management of the effects of MPs on skin health.

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