We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis
Summary
Using computational toxicology and multi-omics analysis, researchers identified three key proteins (AKT1, PIK3CD, and PIM1) through which PET microplastics may promote pulmonary fibrosis, a serious scarring disease of the lungs. The microplastics appear to affect metabolic and inflammatory pathways in specific lung and immune cells. This study provides molecular evidence for how inhaled plastic particles from everyday items could contribute to chronic lung disease.
Polyethylene terephthalate microplastics (PET-MPs) are persistent in the environment and have become an emerging health concern. PET-MPs play a role in lung pathologies; however, little is known about their role in idiopathic pulmonary fibrosis (IPF). Our research aimed to determine the role of PET-MPs in exacerbating IPF by combining improved detection and toxicology. The ProTox 3.0 platform was used to predict the microplastic toxicity of polyethylene terephthalate. The toxicological mechanism of PET-MP-induced IPF was explored using network toxicology, molecular docking, Mendelian randomization, and single-cell sequencing analysis. By analyzing the PubChem, ChEMBL, and SwissTargetPrediction databases, 120 potential targets related to PET-MPs exposure were identified, and 81 intersecting targets were obtained by intersecting the IPF gene in the Gene Expression Omnibus database. These were further optimized into three core targets, namely AKT1, PIM1, and PIK3CD. PET-MPs affected metabolic, lipid, atherosclerosis, and C-type selection receptor signaling pathways. The binding affinity of PET-MPs to these core targets was potent, and PET-MPs had a good binding effect with these target proteins. PET-MPs exhibit lung toxicity, which may be related to three key proteins: AKT1, PIK3CD, and PIM1. PET-MPs may exacerbate IPF via metabolic pathways, lipids, and atherosclerosis, which may occur in AT2 and CD8+T cells. This study offers valuable information on the molecular mechanism of IPF triggered by PET-MPs, emphasizing the practicality of network toxicology in the toxicity evaluation of emerging environmental contaminants.
Sign in to start a discussion.
More Papers Like This
Network toxicology and bioinformatics analysis reveal the molecular mechanisms of polyethylene terephthalate microplastics in exacerbating diabetic nephropathy
This computational study used bioinformatics to explore how polyethylene terephthalate (PET) microplastics might worsen diabetic kidney disease. The analysis identified key genes and inflammatory pathways that are affected by both PET microplastics and kidney damage in diabetes. The findings suggest that microplastic exposure could accelerate kidney problems in people who already have diabetes, though lab and clinical studies are needed to confirm this.
A particle of concern: explored and proposed underlying mechanisms of microplastic-induced lung damage and pulmonary fibrosis
This paper explores how inhaled microplastics may cause lung damage and scarring (pulmonary fibrosis) through several biological pathways. The research identifies signaling pathways that could be targeted for future treatments to reduce microplastic-induced lung damage. This is relevant to human health because people regularly breathe in airborne microplastic particles.
Integration of transcriptomics and metabolomics reveal cytotoxic mechanisms of Polyethylene terephthalate microplastics in BEAS-2B cells
Researchers exposed human lung cells to PET microplastics and used combined gene and metabolite analysis to uncover the mechanisms of toxicity. They found that the microplastics disrupted lipid metabolism and activated cell death pathways, reducing cell viability over time. The study suggests that inhaled PET microplastics could pose risks to respiratory health by triggering harmful molecular changes in lung tissue.
Assessing the toxicological effects of exposure to environmental pollutants PET-MPs on vascular diseases: insights from network toxicology, molecular docking, molecular dynamics, and experimental validation
Researchers used network toxicology, molecular docking, and cell experiments to investigate how PET microplastics may contribute to vascular diseases. They identified four core molecular targets and found that PET microplastics induced mitochondrial oxidative stress, increased reactive oxygen species, and promoted vascular smooth muscle cell death. The study provides initial molecular-level evidence that microplastic exposure may be a contributing factor in vascular damage and remodeling.
Polystyrene nanoplastics and lung cancer: Insights from network toxicology and mechanistic in vitro studies
Network toxicology analysis identified 189 potential molecular targets linking polystyrene nanoplastic exposure to lung cancer pathways, and in vitro experiments confirmed that nanoplastics promote lung cancer cell proliferation and resistance to apoptosis via PI3K/AKT signaling.