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61,005 resultsShowing papers similar to Unveiling the pathogenic mechanisms of polyethylene terephthalate-microplastic-driven osteoarthritis and rheumatoid arthritis: PTGS2 signaling hub-oriented toxicity profiling
ClearIntegrated 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.
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.
Microplastics as an emerging driver of osteoarthritis: a translational synthesis of environmental exposure, patho-mechanisms, and public health implications
A translational synthesis of clinical and experimental data examined the role of microplastic exposure in osteoarthritis (OA) development, finding evidence that MPs bioaccumulate in joint tissues and may promote inflammation and oxidative damage that disrupts cartilage homeostasis. The review identified MP exposure as a plausible but underexplored contributor to OA progression.
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.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Researchers used network toxicology, machine learning, and molecular docking to investigate how PET degradation products—ethylene glycol and terephthalic acid—affect colorectal cancer prognosis through the glucocorticoid signaling pathway. The analysis identified 43 shared target genes, suggesting that PET breakdown products may worsen colorectal cancer outcomes by dysregulating glucocorticoid-mediated anti-inflammatory and cell survival signals.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Combining network toxicology, machine learning, and molecular docking, this study found that PET plastic degradation products ethylene glycol and terephthalic acid may influence colorectal cancer prognosis through 43 shared genes linked to TNF/IL-17 signaling and glucocorticoid-mediated metabolic pathways.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
This computational study investigated how PET microplastic degradation products affect colorectal cancer prognosis, identifying 43 genes linking ethylene glycol and terephthalic acid exposure to cancer pathogenesis via chronic inflammation mediated through TNF/IL-17 and glucocorticoid metabolic pathways.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
Researchers used computational methods including network toxicology, machine learning, and molecular docking to explore how polystyrene microplastics might contribute to childhood obesity. They identified 40 overlapping genes between obesity-related and microplastic-affected pathways, concentrated in lipid metabolism and insulin signaling. The study suggests that polystyrene microplastics may act as environmental triggers capable of disrupting metabolic balance by interacting with key regulatory genes.
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.
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.
Bisphenol A disrupts cartilage homeostasis through dual targeting of TP53 and PTGS2 signaling networks
This network toxicology and molecular docking study found that bisphenol A (a plasticizer found in many plastics) interacts with key osteoarthritis-associated targets including TP53 and PTGS2, suggesting BPA may contribute to cartilage breakdown by disrupting inflammation and apoptosis signaling pathways.
Environmental pollutants as emerging risk factors in osteoarthritis: Mechanistic and epidemiological evidence
This review synthesized mechanistic and epidemiological evidence linking environmental pollutants — including microplastics — to osteoarthritis pathogenesis. The authors found accumulating in vitro, animal, and human data suggesting that chemical exposures accelerate cartilage degradation and joint inflammation through multiple pathways.
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.
Polyethylene terephthalate microplastics exposure enhances the risk of ulcerative colitis: insights from multiomics integration, machine learning, and molecular docking reveal intestinal toxicity mechanisms
Using multiomics integration, machine learning, and molecular docking, this study identified mechanisms by which PET microplastic exposure may increase the risk of ulcerative colitis. Key pathways included intestinal barrier disruption, immune dysregulation, and oxidative stress triggered by PET-MP-protein interactions.
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.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
Researchers used an integrative computational approach combining cross-species transcriptomics, network toxicology, and molecular docking to investigate potential links between polystyrene microplastic exposure and childhood obesity. They identified shared gene targets involved in lipid metabolism and insulin signaling pathways, with molecular docking confirming stable binding between microplastic compounds and key metabolic proteins. The findings provide a preliminary molecular hypothesis suggesting microplastics could disrupt metabolic processes relevant to obesity.
Microplastics aggravates rheumatoid arthritis by affecting the proliferation/migration/inflammation of fibroblast-like synovial cells by regulating mitochondrial homeostasis
Researchers investigated how microplastics affect the joint tissue cells involved in rheumatoid arthritis using lab and animal models. They found that microplastic exposure promoted the growth, spread, and inflammatory activity of these cells, while also worsening cartilage damage through disruption of mitochondrial function. The study suggests that microplastic exposure may aggravate inflammatory joint conditions by interfering with cellular energy processes.
Polystyrene microplastics activate NF-κB/MAPK signaling in synovial fibroblasts, promoting inflammation and joint destruction in rheumatoid arthritis
Researchers detected polystyrene microplastics in synovial fluid from rheumatoid arthritis patients and showed that 5 µm particles directly activated NF-κB and MAPK inflammatory signaling in joint fibroblasts, potentially amplifying synovial inflammation and joint destruction.
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.
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.
Investigating the link between microplastic exposure (benzyl butyl phthalate) and neurodegenerative diseases using high-performance computational toxicology
Researchers used computational toxicology methods to investigate potential links between benzyl butyl phthalate, a plasticizer associated with microplastic exposure, and neurodegenerative diseases. The analysis revealed that this compound has the potential to interact with proteins PRKN and PDK1, which are involved in neurological function. The study suggests a possible molecular mechanism by which microplastic-associated chemicals could contribute to neurodegeneration, though further experimental validation is needed.
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.
Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis
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.
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.