Table 1.

Effects of Microplastics/Nanoplastics on skin tissue and the underlying mechanisms

Model & cell type	MPs type & diameter	Exposure concentration	Exposure duration	Target cell type	Mechanism	Reference
C57BL/6J mice; fibroblasts	Polystyrene (PS), 150 μm	0, 50, 100, 200, 400 µg/mL	24 h	Fibroblasts	Inhibits COL1A1, COL1A2, SPP1 expression, disrupting ECM homeostasis and accelerating skin aging.	[45]
HaCaT cells; C57BL/6 mice	PS, 100 nm	10, 50, 100 µg/mL (cells); 12.5, 25 mg/kg (mice)	24–72 h (cells); 18 days (mice)	HaCaT keratinocytes	Induces mitochondrial oxidative stress, GSDMD-mediated mtDNA release, activating AIM2 inflammasome and triggering inflammation and cellular senescence.	[46]
HaCaT, SCL-1, A431 cells	Polyethylene (PE), 1 μm	0.25, 0.5, 1 mg/mL	24 h	HaCaT and SCC cells	Increases mitochondrial ROS and membrane potential changes, activating NLRP3 via mtDNA leakage and promoting proliferation of skin cancer cells.	[47]
Dermal fibroblasts and keratinocytes from SKH1-hr mice	Fluorocarbon (FB) PS, 200 nm–6 μm	100 µg/mL	24 h	Fibroblasts and keratinocytes	Enhances intracellular ROS, activates Nrf2-dependent antioxidant response, and alters β-catenin signaling.	[48]
C57BL/6 mice; HaCaT, L929 cells	Aged PS, 120 nm	30 mg/kg (mice); 24 h (cells); 60 days (mice)	24 h (cells). 60 days (mice)	HaCaT and L929 cells	Exacerbates toxicity in skin and follicular cells, induces mitochondrial apoptosis, disrupts follicle-shaft adhesion, leading to hair loss.	[49]