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61,005 resultsShowing papers similar to Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis
ClearNetwork 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.
Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation
Researchers used network toxicology analysis and laboratory experiments to investigate how polyethylene terephthalate microplastics may contribute to atherosclerosis. They identified several molecular targets and biological pathways through which these microplastics could promote plaque formation in blood vessels. The study provides preliminary evidence that a commonly encountered type of microplastic may interact with cardiovascular disease mechanisms, though further research is needed to confirm these findings.
Exploring the Potential Mechanism of Polyethylene Terephthalate Associated Cardiotoxicity through Network Toxicology and Molecular Docking
Researchers used computational approaches including network toxicology, molecular docking, and molecular dynamics simulations to explore how polyethylene terephthalate microplastics may affect cardiovascular function. The study identified potential molecular pathways through which PET exposure could contribute to cardiotoxicity. The findings provide a theoretical framework for understanding how plastic contaminants might interact with heart-related biological targets.
Assessing the toxicological impact of PET-MPs exposure on IVDD: Insights from network toxicology and molecular docking
Using computer modeling and molecular analysis, researchers identified key biological targets through which PET microplastics (the type found in plastic bottles) may contribute to spinal disc degeneration. The study found that PET particles could disrupt immune pathways, cell death processes, and tissue breakdown, suggesting a potential link between microplastic exposure and degenerative spinal conditions.
In silico insights into microplastic additive toxicity: Risks of pulmonary fibrosis and endocrine disruption
Researchers used computational modeling to investigate how five common microplastic additives, including phthalates and flame retardants, interact with proteins involved in lung fibrosis and endocrine function. Molecular docking revealed that these additives bind strongly to fibrotic markers like TGF-beta and to hormone receptors, suggesting potential mechanisms for tissue damage and hormonal disruption. The study highlights the need for further investigation into the health risks posed by chemical additives leaching from microplastics.
The impact of polyethylene terephthalate microplastics on the pathogenesis of atherosclerosis: Focusing on network toxicology and target gene detection
Researchers used network toxicology and gene analysis to investigate how PET microplastics may influence atherosclerosis, the buildup of plaque in arteries. They identified specific genes involved in inflammation and immune cell signaling that are affected by both PET exposure and atherosclerosis development. The study suggests that microplastic exposure could worsen cardiovascular disease through shared inflammatory pathways.
Elucidating the Mechanism of Polyethylene Terephthalate Micro / Nanoplastics Inducing Gestational Diabetes Mellitus through Network Toxicology and Molecular Docking Analysis
Researchers used computer modeling to investigate how tiny plastic particles shed from PET water bottles and packaging may contribute to gestational diabetes, identifying three key regulatory proteins (STAT1, PIK3R1, PTPN11) that PET microplastics appear to disrupt. The findings suggest these particles could interfere with insulin signaling during pregnancy, pointing to a potential environmental driver of a condition that affects millions of expectant mothers.
Microplastic exposure and allergic rhinitis: Network toxicology, and molecular docking insights
Researchers used network toxicology and molecular docking approaches to investigate how microplastic exposure may contribute to allergic rhinitis. The study identified key molecular mediators through which microplastics may drive respiratory inflammation pathways, and found that resveratrol could potentially modulate these pathways, offering insights into the mechanisms linking microplastic exposure to allergic respiratory conditions.
The toxicological impact of PET-MPs exposure on atherosclerosis: insights from network toxicology, molecular docking, and machine learning
Researchers used network toxicology, molecular docking, and machine learning to identify how PET microplastics may promote atherosclerosis, narrowing 28 candidate targets to seven key genes and predicting interactions with atherosclerosis-relevant pathways including inflammation and lipid metabolism.
Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage
This study found that polypropylene nanoplastics, one of the most common types of plastic particles, can cause lung inflammation by damaging mitochondria (the energy-producing parts of cells) and triggering inflammatory signaling pathways. These findings suggest that breathing in tiny plastic particles could contribute to lung disease through a specific chain of cellular damage.
Integrated network toxicology, machine learning, molecular docking and experimental validation to elucidate mechanism of polyethylene terephthalate microplastics inducing periodontitis
Researchers combined computational biology, machine learning, and laboratory experiments to explore how polyethylene terephthalate microplastics might contribute to periodontitis, a common gum disease. They identified key molecular targets and signaling pathways through which microplastics could promote gum tissue inflammation. The study provides the first evidence linking microplastic exposure to the biological mechanisms underlying periodontal disease.
The Effect of Subchronic Polyethylene Microplastic Exposure on Pulmonary Fibrosis Through Pro-Inflammatory Cytokines TNF-α and IL-1β in Wistar Rats
This animal study found that breathing in polyethylene microplastics over several weeks led to lung scarring (pulmonary fibrosis) in rats by triggering inflammatory immune responses. The results suggest that chronic inhalation of airborne microplastics could contribute to serious lung damage in humans, since we breathe in thousands of plastic particles daily.
Microplastics as environmental modifiers of lung disease
This review examines growing evidence that inhaled microplastics may contribute to lung diseases including asthma, pulmonary fibrosis, and chronic obstructive pulmonary disease. Researchers found that different plastic types, sizes, and weathering states can trigger inflammation, oxidative stress, and cellular changes in lung tissue, suggesting microplastics may act as environmental modifiers that worsen respiratory conditions.
Multi-Omics Analysis Reveals the Toxicity of Polyvinyl Chloride Microplastics toward BEAS-2B Cells
Researchers used advanced gene and metabolite analysis to reveal how PVC microplastics damage human lung cells. Exposure altered the expression of 530 genes and nearly 4,000 metabolites, particularly disrupting fat metabolism pathways and activating inflammatory stress responses. These findings are important because airborne PVC microplastics are common in indoor and outdoor environments, and the study reveals specific biological pathways through which inhaled microplastics could contribute to lung disease.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
Environmental PET-microplastic exposure and risk of non-alcoholic fatty liver disease: An integrated computational toxicology and multi-omics study
Researchers used computational toxicology and machine learning to identify six key genes linking PET microplastic exposure to non-alcoholic fatty liver disease (NAFLD), with the model achieving high diagnostic accuracy and molecular docking suggesting that PET-derived chemicals may directly bind to proteins controlling liver fat metabolism.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
Molecular interactions and dynamics of microplastics in indoor dust with lung-inflammatory receptors: A study in academic settings
Researchers used molecular simulation to study how microplastics in indoor dust interact with lung-lining lipid molecules, finding that MP surfaces adsorb lung surfactant components in ways that could impair pulmonary surfactant function and increase inflammatory signaling after inhalation.
Intersection of microplastic toxicity targets and differentially expressed genes in allergic rhinitis.
Network analysis identified a set of genes that are both targeted by common microplastics (PE, PP, PVC, PS) and differentially expressed in allergic rhinitis, providing a molecular framework for investigating how microplastic exposure may contribute to nasal allergy pathogenesis.
Exposure to Polyethylene Terephthalate Microplastic Induces Mouse Liver Fibrosis Through Oxidative Stress and p38 MAPK/p65 NF‐κB Signaling Pathway
Researchers found that exposure to PET microplastics induced liver fibrosis in mice through oxidative stress and activation of the p38 MAPK/p65 NF-kB signaling pathway. The study suggests that PET microplastics, which are frequently detected in both environmental samples and human tissues, may contribute to liver damage through inflammatory and oxidative mechanisms.