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Microplastics impair wound healing via NAT10-mediated epigenetic dysregulation of FASN-PI3K/AKT signaling
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Researchers found that microplastic exposure significantly delayed wound healing in both diabetic and non-diabetic mice, with transcriptomic analysis revealing that microplastics suppress the wound healing pathway through NAT10-mediated epigenetic regulation of FASN-PI3K/AKT signaling, with stronger effects in diabetic animals.
Microplastics (MPs) are environmental pollutants with potential health risks. This study examined the effect of MPs on wound healing in both diabetic and non-diabetic mice. MPs exposure significantly delayed wound healing, particularly in diabetic mice, with reduced epidermal thickness and impaired collagen deposition. Mechanistically, MPs suppressed cell proliferation, angiogenesis, and increased apoptosis. Transcriptomic analysis identified dysregulation of critical wound healing pathways, especially those involved in inflammation, extracellular matrix remodeling, and lipid metabolism. Notably, the PI3K/AKT signaling pathway was inhibited. In vitro experiments using human dermal fibroblasts confirmed that MPs disrupted the PI3K/AKT pathway, reducing cell proliferation and migration. Further investigation revealed that MPs suppressed N-acetyltransferase 10 (NAT10) expression, leading to reduced ac4C-dependent stabilization of Fasn mRNA, which in turn diminished lipid synthesis and further inhibited the PI3K/AKT pathway. Our findings reveal a novel interaction between MPs and diabetes in impairing wound healing and suggest the NAT10-FASN-PI3K/AKT axis as a potential therapeutic target.
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Nanoplastic-induced NAT10/ac4C axis drives both oxidative stress and chemoresistance
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Researchers discovered that polystyrene nanoplastics trigger an epitranscriptomic stress response in cells by activating the enzyme NAT10, which hypermodifies transfer RNA with N4-acetylcytidine (ac4C) marks — and found this same pathway also reduces the effectiveness of the cancer drug sorafenib by nearly fourfold, establishing a direct link between nanoplastic exposure and impaired chemotherapy response.
Microplastics cause hepatotoxicity in diabetic mice by disrupting glucolipid metabolism via PP2A/AMPK/HNF4A and promoting fibrosis via the Wnt/β‐catenin pathway
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Researchers found that microplastic exposure caused liver damage in diabetic mice by disrupting the way the liver processes sugars and fats through specific cellular signaling pathways. The microplastics also promoted liver scarring through activation of a fibrosis-related pathway. The study suggests that individuals with existing metabolic conditions like diabetes may be particularly vulnerable to the harmful effects of microplastic accumulation in the body.
Cellular mechanisms of microplastic and nanoparticle exposure and its relationship with metabolic diseases: Literature review
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This literature review examined how microplastic and nanoparticle exposure affects cellular mechanisms related to metabolic disease, finding evidence that these contaminants disrupt insulin signaling, alter lipid metabolism, and may contribute to the development of metabolic syndrome.
Mixtures of polystyrene micro and nanoplastics affects fat and glucose metabolism in 3T3-L1 adipocytes and zebrafish larvae
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Exposure to a mixture of micro- and nanoplastics increased fat production and impaired the body's ability to use insulin and process sugar in both cell and zebrafish experiments. The plastic mixture triggered inflammation, boosted fat-storing genes, and suppressed insulin signaling pathways. These findings suggest that microplastic exposure could contribute to obesity and type 2 diabetes.
PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-β1/Smad2/3 signaling pathways.
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In a mouse model of diabetic nephropathy, polystyrene microplastic exposure worsened kidney inflammation and fibrosis by activating the NLRP3/Caspase-1 and TGF-beta1/Smad2/3 signaling pathways, suggesting microplastics may accelerate progression of this common diabetic complication.
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