We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Microplastics and Skin Aging: Disruption of Barrier Function and Induction of Fibroblast Senescence
AI summary Read the abstract
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.
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.
More Papers Like This
Nano-sized microplastics exposure induces skin cell senescence via triggering the mitochondrial localization of GSDMD
AI summary Read the abstract
Researchers found that nano-sized microplastics enter skin cells and trigger premature aging (senescence) by damaging the energy-producing structures inside cells (mitochondria) and activating inflammatory pathways. This study suggests that microplastic exposure could accelerate skin aging and inflammation, adding to concerns about the health effects of plastic pollution on organs exposed to the environment.
Microplastics, Skin Disease, and Dermatology
AI summary Read the abstract
This review examined the risks that microplastics and nanoplastics pose to skin health, noting that particles can penetrate compromised skin barriers and cause oxidative stress, inflammation, and cellular senescence in fibroblasts. The authors recommend that dermatologists incorporate microplastic exposure into clinical assessments of skin conditions.
Deciphering the links: Fragmented polystyrene as a driver of skin inflammation
AI summary Read the abstract
Researchers tested fragmented polystyrene particles on human skin using cell cultures, live mice, and donated human skin samples, finding that these microplastics can penetrate skin layers and trigger significant inflammation. The particles were taken up by skin cells and caused the release of inflammatory signals, suggesting that everyday skin contact with microplastics in cosmetics, textiles, and dust could contribute to skin irritation and inflammatory skin conditions.
Measuring the toxicological ramifications of MNP exposure on skin senescence: Insights gained through network toxicology and transcriptomic analysis
AI summary Read the abstract
Using network toxicology and transcriptomics, researchers found that polystyrene microplastic exposure triggered skin cell senescence through oxidative stress pathways, with MNP-PS targeting 92% of known MNP-associated genes and activating beta-galactosidase and ROS-mediated senescence markers.
Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells
AI summary Read the abstract
Researchers found that microplastic exposure accelerates aging in fat tissue by triggering cellular senescence (a state where cells stop dividing and release inflammatory signals) in both mice and cell cultures. The microplastics accumulated in fat tissue, increased markers of aging and inflammation, and disrupted the normal development of new fat cells. These findings suggest that chronic microplastic exposure could contribute to age-related metabolic problems and obesity-related diseases in humans.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.