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61,005 resultsShowing papers similar to Detection of the Disorders of Glycerophospholipids and Amino Acids Metabolism in Lung Tissue From Male COPD Patients
ClearTargeted metabolomics reveals differential biological effects of nanoplastics and nanoZnO in human lung cells
Researchers used targeted metabolomics to compare how nanoplastics and zinc oxide nanoparticles affect human lung cells at the molecular level. Even at concentrations that did not cause obvious cell death, both types of nanoparticles significantly disrupted cell metabolism, though through different biochemical pathways. The study suggests that standard toxicity tests may underestimate the harmful effects of nanoplastics on human respiratory cells.
A metabolomics perspective on the effect of environmental micro and nanoplastics on living organisms: A review
This review examines how scientists use metabolomics, the study of small molecules produced by cellular processes, to understand the toxic effects of microplastics and nanoplastics on living organisms. The research shows that these plastic particles disrupt metabolism in consistent ways across species, affecting energy production, fat processing, and amino acid pathways. These shared metabolic disruptions across different organisms suggest that microplastics could cause similar metabolic problems in humans.
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.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
Investigation of the presence of microplastics and their clinical significance in patients with exacerbation and stable periods of chronic obstructive pulmonary disease
Researchers examined the presence of microplastics in sputum and bronchoalveolar lavage samples from chronic obstructive pulmonary disease (COPD) patients during exacerbation and stable phases. MPs were detected in a majority of patient samples, and their presence was associated with greater airway inflammation, suggesting inhaled microplastics contribute to COPD pathology.
A Review of Liquid Chromatography-Mass Spectrometry Strategies for the Analyses of Metabolomics Induced by Microplastics
This review summarized liquid chromatography-mass spectrometry strategies for analyzing metabolomic changes induced by microplastic exposure, covering analytical approaches for understanding how microplastics disrupt metabolic pathways in living organisms.
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.
Phospholipidomics in Clinical Trials for Brain Disorders: Advancing our Understanding and Therapeutic Potentials
Researchers reviewed how phospholipidomics — the detailed study of fatty molecules called phospholipids in the brain — is advancing the understanding and diagnosis of neurological diseases like Alzheimer's and Parkinson's. Specific phospholipid patterns may serve as early biomarkers, potentially leading to better diagnostic tools and targeted treatments.
Comparative Metabolomic Approaches to Nanoplastic Toxicity in Mammalian and Aquatic Systems
This review compared metabolomic approaches used to characterize nanoplastic toxicity across mammalian and aquatic biological systems, synthesizing data on oxidative stress, mitochondrial dysfunction, and metabolic pathway disruption. The authors found convergent metabolic signatures—particularly in amino acid and lipid metabolism—across diverse organisms, suggesting common toxicological mechanisms regardless of species.
Metabolomics reveals the toxicity of polystyrene nanoplastics in the gills of Acrossocheilus yunnanensis
Researchers used metabolomics to study how polystyrene nanoplastics affect the gills of the freshwater fish Acrossocheilus yunnanensis. They found that nanoplastic exposure caused oxidative stress, tissue lesions, and significant disruption of lipid metabolism, particularly glycerophospholipid and sphingolipid pathways. The study suggests that nanoplastics primarily harm fish gills by damaging tissue integrity and disrupting the lipid balance that maintains cell membrane function.
Potential toxicity of micro- and nanoplastics in primary bronchial epithelial cells of patients with chronic obstructive pulmonary disease
Researchers investigated how micro- and nanoplastics affect lung cells taken from patients with chronic obstructive pulmonary disease (COPD), a condition that already impairs breathing. The study aimed to determine whether plastic particle exposure poses additional toxic risk to people whose airways are already compromised.
Role of mitochondria-associated membranes (MAMs) in inflammatory signaling: implications for acute lung injury pathogenesis
This review examines how dysfunction of mitochondria-associated membranes — contact zones between the endoplasmic reticulum and mitochondria — contributes to inflammatory signaling and acute lung injury pathogenesis through dysregulated calcium signaling, lipid metabolism, and inflammatory activation.
Exposure to environmental xenobiotics and lung tissue function: A comprehensive review on biological mechanisms and pathways
This comprehensive review examines how environmental pollutants including microplastics, heavy metals, and volatile organic compounds damage lung tissue through mechanisms like oxidative stress, inflammation, and disruption of cellular barriers. The study suggests these pollutants contribute to chronic respiratory diseases and highlights how they can also cause epigenetic changes that may affect future generations.
The Effects of Immunosuppression on the Lung Microbiome and Metabolites in Rats
Researchers investigated the lung microbiome and metabolites in immunosuppressed rats to clarify whether pneumonia in this population arises from inhaled oropharyngeal pathogens or abnormal proliferation of pulmonary proteobacteria. The study used a cyclophosphamide-induced immunosuppression model to characterize shifts in the respiratory microbial community.
Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells
Researchers exposed normal human liver and lung cells to 80-nanometer plastic particles and found that the nanoplastics damaged mitochondria, the energy-producing structures inside cells, without causing widespread cell death. Using metabolomics analysis, they identified specific disruptions to energy metabolism and lipid processing pathways in both cell types. This study reveals a subtle but important way that nanoplastics could impair organ function in humans by disrupting cellular energy production.
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.
Epigenetic regulation of pulmonary inflammation
Researchers reviewed how environmental exposures drive epigenetic changes — including DNA methylation, histone modifications, and non-coding RNA transfers via extracellular vesicles — that promote chronic lung diseases such as COPD, asthma, and pulmonary fibrosis, while also identifying these same epigenetic pathways as promising therapeutic targets.
Mitochondrial Dysfunction and Nanocarrier-Based Treatments in Chronic Obstructive Pulmonary Disease (COPD)
This review examines how mitochondrial dysfunction contributes to the development and progression of chronic obstructive pulmonary disease. Researchers highlight emerging nanocarrier-based drug delivery systems designed to target mitochondrial dysfunction in lung tissue. The study suggests these novel nanoparticle approaches, while still in early clinical stages, represent a promising direction for future treatments.
Expression Profiles of circRNAs and Identification of hsa_circ_0007608 and hsa_circ_0064656 as Potential Biomarkers for COPD-PH Patients
This study identified expression profiles of circular RNAs in COPD-related pulmonary hypertension and identified two candidates (hsa_circ_0007608 and hsa_circ_0064656) as potential diagnostic biomarkers or therapeutic targets.
PET microplastics induce lipotoxicity in the porcine pancreas
Researchers used proteomic analysis to study the effects of PET microplastics on the porcine pancreas after four weeks of exposure at low and high doses. The study found that PET microplastics induced lipotoxicity in the pancreas, disrupting lipid metabolism pathways and suggesting that microplastic ingestion may affect pancreatic function through altered protein expression profiles.
A bibliometric analysis of autophagy in lung diseases from 2012 to 2021
This bibliometric analysis maps autophagy research in lung diseases from 2012 to 2021, identifying key research hotspots, collaboration networks, and emerging trends linking autophagy mechanisms to various pulmonary conditions.
Deposition of microplastics associated with bioaccumulation of heavy metals in human lungs of smokers: Implications of adsorption and mobilization of metals via microplastics
Researchers compared lung tissue from smokers and non-smokers and found that smokers accumulated more microplastics alongside elevated levels of heavy metals in lung tissue, suggesting that tobacco smoke enhances chelation of heavy metals to airborne microplastics, increasing lung bioaccumulation.
PET microplastics induce lipotoxicity in the porcine pancreas
Researchers used proteomic analysis to study the effects of PET microplastics on the porcine pancreas after four weeks of exposure at low and high doses. The study found that PET microplastics induced lipotoxicity in the pancreas, disrupting lipid metabolism pathways and suggesting that microplastic ingestion may affect pancreatic function through altered protein expression profiles.
The impaired response of nasal epithelial cells to microplastic stimulation in asthma and COPD
Researchers exposed nasal lining cells from healthy people, asthma patients, and COPD patients to polyamide microplastic fibers and found that diseased airways responded very differently than healthy ones. Asthma cells showed changes in cholesterol metabolism and stress responses, while COPD cells showed altered immune cell movement and signaling. This suggests that people with existing respiratory conditions are more vulnerable to the harmful effects of inhaled microplastic fibers.