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20 resultsShowing papers similar to Acute Endoplasmic Reticulum Stress Induces Inflammation Reaction, Complement System Activation, and Lipid Metabolism Disorder of Piglet Livers: A Proteomic Approach
ClearEndoplasmic Reticulum Stress-related Classification for Prognosis Prediction in Hepatocellular Carcinoma
Researchers used gene expression data to create an endoplasmic reticulum stress-based classification system for predicting outcomes in liver cancer patients. The model identified patient subgroups with significantly different survival rates.
Endoplasmic reticulum stress exacerbates microplastics-induced toxicity in animal cells
Researchers investigated how microplastic exposure affects animal cells through a stress response in a cellular structure called the endoplasmic reticulum. They found that microplastics triggered this stress pathway, which amplified toxic effects including inflammation and cell death. The study suggests that endoplasmic reticulum stress may be an important and previously underappreciated mechanism through which microplastics cause damage to tissues.
Nanoplastic propels diet-induced NAFL to NASH via ER-mitochondrial tether-controlled redox switch
Researchers investigated how nanoplastic exposure may accelerate the progression of diet-induced fatty liver conditions in animal models. The study found that nanoplastics disrupted the connections between the endoplasmic reticulum and mitochondria, triggering oxidative stress responses that worsened liver inflammation and damage.
Microplastics induced endoplasmic reticulum stress to format an inflammation and cell death in hepatocytes of carp (Cyprinus carpio)
Researchers fed carp water containing polystyrene microplastics and found significant liver damage, including inflammation, disrupted cell recycling processes, and cell death. The microplastics triggered a stress response in the cell's protein-folding machinery (endoplasmic reticulum), which set off a chain reaction of inflammation and tissue damage. These findings in freshwater fish suggest that microplastics can cause serious organ damage through specific cellular stress pathways.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.
Nanoplastic Exposure at Environmental Concentrations Disrupts Hepatic Lipid Metabolism through Oxidative Stress Induction and Endoplasmic Reticulum Homeostasis Perturbation
A study in fish found that nanoplastics at environmentally realistic concentrations accumulated in the liver and disrupted fat metabolism, causing a condition similar to fatty liver disease. Smaller nanoplastics (100 nanometers) caused more severe damage than larger microplastics by disrupting protein processing in cells and triggering oxidative stress. These findings raise concerns that nanoplastics in the environment could affect liver health in fish and potentially in humans who consume contaminated seafood.
Endoplasmic Reticulum Stress-Related Signature for Predicting Prognosis and Immune Features in Hepatocellular Carcinoma
Researchers developed a four-gene endoplasmic reticulum stress-based prognostic model for hepatocellular carcinoma using bioinformatics approaches, finding that higher risk scores correlated with advanced tumor stage, HBV infection, and worse survival outcomes. The model also predicted differences in immune cell infiltration profiles, suggesting potential utility for guiding immunotherapy decisions.
Endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens
Researchers exposed chickens to polystyrene microplastics for 42 days and found significant lung damage, including tissue inflammation and cell stress responses. The microplastics triggered a chain reaction starting with stress in the endoplasmic reticulum (a cell structure involved in protein processing) that activated inflammatory pathways. While this study focused on poultry, similar inflammatory mechanisms could be relevant to understanding how microplastics affect lungs in other species, including humans.
PET microplastics alter the transcriptome profile and oxidative stress markers in the liver of immature piglets: an in vivo study
Researchers fed immature piglets PET microplastics for four weeks and examined the effects on their livers. They found that microplastic exposure altered gene expression patterns related to metabolism and immune response, and increased markers of oxidative stress in the liver. The study suggests that even relatively short-term microplastic ingestion may disrupt liver function at the molecular level.
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.
Zebrafish exposure to high-density polyethylene and polystyrene microplastics: effects on liver transcriptome and gastrointestinal histology
This study used proteomics — the analysis of all proteins expressed by cells — to identify how zebrafish respond to exposure to high-density polyethylene and polystyrene microplastics, finding disruption of proteins involved in metabolism, oxidative stress, and immune defense. The protein-level analysis complements genomic approaches and reveals the biological mechanisms underlying microplastic toxicity in fish.
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.
PET microplastics induce lipotoxicity in the porcine pancreas
Researchers exposed pigs to PET microplastics for four weeks and found dose-dependent changes in pancreatic protein profiles, with the higher dose altering 17 proteins involved in fatty acid synthesis, lipid peroxidation, and digestive enzyme production. Free fatty acid levels increased significantly at the higher dose, indicating lipotoxic stress in pancreatic tissue. The study suggests a novel pathway through which microplastics may contribute to metabolic disturbances by impairing pancreatic function.
The involvement of oxidative stress mediated endoplasmic reticulum pathway in apoptosis of Golden Pompano (Trachinotus blochii) liver under PS-MPs stress
Researchers exposed golden pompano, a commercially important marine fish in China, to polystyrene microplastics at three concentrations for 14 days and observed slowed growth and significant liver damage. The microplastics induced oxidative stress and triggered endoplasmic reticulum-mediated apoptosis in liver cells. The study provides evidence that coastal aquaculture species face real toxicological risks from microplastic pollution in their farming environments.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Proteomic and lipidomic profiling of mouse livers after polypropylene microplastic exposure revealed crosstalk between hepatic lipid fluctuations, nutrient metabolism disorders, and energy pathway disarrangements, providing mechanistic insight into microplastic-induced liver toxicity.
Evaluation of nanoplastics toxicity in the soil nematode Caenorhabditis elegans by iTRAQ-based quantitative proteomics
Researchers used quantitative proteomics to evaluate nanoplastic toxicity in the nematode C. elegans, identifying disrupted proteins involved in oxidative stress, metabolism, and cellular defense pathways, providing molecular-level insight into how nanoplastics harm organisms.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death
This review examines how endoplasmic reticulum stress, a cellular response to accumulated misfolded proteins, can trigger various forms of cell death in acute kidney injury. While not directly about microplastics, these same stress pathways are activated when cells are exposed to nanoplastics, which have been shown to accumulate in kidney tissue. Understanding these mechanisms helps explain how microplastic exposure could contribute to kidney damage at the cellular level.
Investigating Polystyrene Nano-Plastic Effects on Largemouth Bass (Micropterus salmoides) Focusing on mRNA Expression: Endoplasmic Reticulum Stress and Lipid Metabolism Dynamics
Researchers investigated how polystyrene nanoplastics affect the liver of largemouth bass, focusing on endoplasmic reticulum stress and fat metabolism. They found that nanoplastic exposure disrupted normal lipid processing and triggered stress responses in liver cells, altering the expression of genes involved in fat storage and energy regulation. The study suggests that nanoplastic pollution in freshwater environments may impair metabolic health in fish.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers examined polypropylene microplastic retention in mouse liver using lipidomics and transcriptomics, finding that chronic exposure disrupted lipid metabolism, cholesterol turnover, and antioxidant defense, with high-dose treatment causing regional liver fibrosis.