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61,005 resultsShowing papers similar to PET-Microplastics Trigger Endothelial Glycocalyx Loss via ER Stress and ROS Unleashing IL-1β-Driven SMC Switching and Early Aortic Structural Impairment
ClearPET-Microplastics Trigger Endothelial Glycocalyx Loss via ER Stress and ROS Unleashing IL-1β-Driven SMC Switching and Early Aortic Structural Impairment
Chronic oral exposure of rats to PET microplastics at 1–100 mg/L caused endothelial glycocalyx loss and structural damage to aortic elastic fibers, with MPs accumulating in vascular tissue. Mechanistically, PET-MPs triggered ER stress and reactive oxygen species production, driving an IL-1β-mediated switch in smooth muscle cell phenotype and early arterial injury.
PET-microplastics trigger endothelial glycocalyx loss via ER stress and ROS unleashing IL-1β-driven SMC switching and early aortic structural impairment
Scientists found that tiny plastic particles from bottles and food packaging can damage blood vessels when consumed regularly. In lab rats, these microplastics caused harmful changes to the cells lining arteries, which could lead to heart disease over time. This research suggests that plastic pollution may pose a direct threat to our cardiovascular health, though more studies are needed to confirm the effects in humans.
The Effect of Modern Lifestyle on Cardiovascular Health
This study found that PET microplastics impaired endothelial cell function by disrupting the SIRT1-eNOS-ROS balance, and that SIRT1 activation (as occurs during exercise) partially protected endothelial cells from PET-induced damage — linking plastic exposure to cardiovascular disease risk mechanisms.
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.
The Effect of Modern Lifestyle on Cardiovascular Health
Researchers investigated how PET microplastics affect vascular endothelial function and tested whether Sirtuin 1 (SIRT1) could provide protection against PET-induced damage in human umbilical vein endothelial cells. PET exposure impaired endothelial function and increased inflammation, while SIRT1 activation partially restored vascular health markers.
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.
Potential mechanisms of aortic medial degeneration promoted by co-exposure to microplastics and lead
Researchers found that microplastics and lead were both present in tissue samples from patients with aortic disease, and in mice, combined exposure to both pollutants caused significant damage to the aorta -- the body's main artery. The co-exposure triggered a form of cell death in blood vessel muscle cells through oxidative stress and mitochondrial damage. This suggests that microplastics may worsen the cardiovascular effects of heavy metals people are already exposed to.
Exposure to polyethylene terephthalate micro(nano)plastics exacerbates inflammation and fibrosis after myocardial infarction by reprogramming the gut and lung microbiota and metabolome
Researchers found that PET microplastics and nanoplastics, one of the most common plastic types found in human coronary blood, worsen heart damage after a heart attack. The plastic particles activated an inflammatory pathway (NLRP3) and disrupted the balance of gut and lung bacteria, leading to chronic inflammation and increased scarring of heart tissue. These findings suggest that plastic pollution exposure may make recovery from heart attacks more difficult.
Virgin and photo-degraded microplastics induce the activation of human vascular smooth muscle cells
Lab tests showed that common microplastics from food packaging (polyethylene and polystyrene) can activate human blood vessel smooth muscle cells in ways linked to atherosclerosis and vascular calcification. Photo-degraded microplastics -- the weathered kind found in the real environment -- triggered even stronger inflammatory responses, suggesting that environmental plastic pollution could contribute to cardiovascular disease.
Potential Effects of Orally Ingesting Polyethylene Terephthalate Microplastics on the Mouse Heart
This study found that mice fed PET microplastics (the type of plastic used in water bottles and food containers) developed heart damage, including broken muscle fibers, significant scarring, and cell death in heart tissue. The damage was driven by a buildup of harmful oxygen molecules (oxidative stress) that overwhelmed the heart's natural defenses. These findings raise concern about the potential cardiovascular effects of PET microplastics that humans commonly encounter in food and drink packaging.
Polyethylene terephthalate microplastics impair erectile function through macrophage mediated cGAS-STING ferroptosis
Researchers investigated the impact of PET microplastic exposure on erectile function using human tissue samples, a rat model, and cell assays. The study found that patients with erectile dysfunction had higher microplastic burden in corpus cavernosum tissue, and that chronic PET microplastic exposure in rats triggered a specific inflammatory pathway involving macrophage ferroptosis that led to vascular dysfunction.
Micro and Nano-plastic particles: What are they and do they effect cardiovascular health?
This review examines the cardiovascular health effects of micro- and nanoplastics, summarizing evidence that these particles have been detected in human tissues including arterial plaques and may promote endothelial dysfunction and inflammation. The authors call for further clinical and epidemiological research into cardiac risk.
Multi-omics analysis reveals size-dependent toxicity and vascular endothelial cell injury induced by microplastic exposurein vivoandin vitro
Researchers used multi-omics analysis to reveal that microplastics cause size-dependent toxicity and injury to vascular endothelial cells both in vivo and in vitro, identifying the vascular system as a previously understudied target of microplastic exposure.
Uterine Microvascular Dysfunction After Plastic Particle Inhalation
Researchers investigated uterine microvascular reactivity in female Sprague Dawley rats after acute inhalation of aerosolized plastic particles to assess cardiovascular effects of micro- and nanoplastic exposures. The study aimed to define mechanisms of microvascular dysfunction caused by plastic aerosols, building on prior epidemiological work linking airborne particulate matter to adverse cardiovascular outcomes.
Microplastics. a New Risk Factor for Atherosclerotic Cardiovascular Disease
This paper reviews emerging evidence linking microplastic exposure to atherosclerotic cardiovascular disease, noting that MPs have been detected in arterial plaques and human tissues and may contribute to cardiovascular risk through inflammation, oxidative stress, and endothelial disruption.
Virgin and Aged Microplastics Induce Type-specific Inflammatory Responses on Vascular Cells
Both virgin and UV-aged polystyrene and polyethylene microplastics triggered inflammatory responses in human coronary artery smooth muscle cells in vitro, with different polymer types and aging states producing distinct patterns of cellular damage. The results suggest that microplastics ingested or inhaled by people may contribute to vascular inflammation and worsen cardiovascular disease — a significant human health concern.
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.
From Environment to Endothelium: The Role of Microplastics in Vascular Aging
This review examines how microplastics may contribute to vascular aging and cardiovascular problems. Evidence indicates that once microplastics enter the body through ingestion, inhalation, or skin contact, they can reach blood vessels and trigger oxidative stress, inflammation, and damage to the cells lining blood vessel walls. The findings suggest that chronic microplastic exposure could be an underappreciated factor in the development of age-related cardiovascular issues.
Toxic effects of nanoplastics on a model of dog aortic cells
Researchers exposed dog aortic endothelial cells to nanoplastic fragments and observed that the particles entered cells and localized in the cytoplasm. The nanoplastics disrupted cell proliferation and metabolic activity while inducing oxidative stress through increased reactive oxygen species production. The study suggests that nanoplastics can directly damage vascular cells, raising questions about potential cardiovascular effects of nanoplastic exposure.
The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats
Researchers exposed rats to polystyrene microplastics at varying doses and examined the effects on heart tissue. They found that microplastic exposure triggered inflammatory cell death and oxidative stress in heart cells through a specific signaling pathway, suggesting that microplastics may pose risks to cardiovascular health.
Fluorescent visualization of endoplasmic reticulum stress induced by microplastic pollution via surge of intracellular reactive oxygen species
Researchers used peroxynitrite as a fluorescent probe to visualize how microplastics trigger endoplasmic reticulum (ER) stress inside cells, finding that MP invasion causes a surge in reactive oxygen species that activates ER stress pathways. The study clarified a key molecular mechanism linking microplastic internalization to cellular disease processes.
Endoplasmic reticulum stress-controlled autophagic pathway promotes polystyrene microplastics-induced myocardial dysplasia in birds
Researchers exposed chicks to different concentrations of polystyrene microplastics to study their effects on heart development. The study found that microplastics triggered endoplasmic reticulum stress and disrupted autophagy pathways in cardiac tissue, leading to myocardial dysplasia in exposed birds.
Ox-LDL induced endothelial progenitor cells oxidative stress via p38/Keap1/Nrf2 pathway
This cell biology study investigated how oxidized low-density lipoprotein (ox-LDL) triggers oxidative stress and cell death in endothelial progenitor cells through a specific signaling pathway. While not directly about microplastics, the study is relevant because microplastics are known to trigger similar oxidative stress pathways in cardiovascular tissues.
Nanoplastics induced oxidative stress and VEGF production in aortic endothelial cells
Researchers exposed aortic endothelial cells to nanoplastics and found that the particles were taken up by the cells and triggered increased production of reactive oxygen species and a growth factor called VEGF, which is involved in blood vessel formation. The nanoplastics also increased metabolic activity while disrupting the cells' antioxidant defenses. The study suggests that nanoplastic exposure may contribute to vascular stress and cardiovascular risk.