We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to Nanoplastics induced oxidative stress and VEGF production in aortic endothelial cells
ClearToxic 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.
Evaluation of toxicity of polystyrene microplastics under realistic exposure levels in human vascular endothelial EA.hy926 cells
Researchers exposed human vascular endothelial cells to polystyrene microplastics at concentrations comparable to levels detected in human blood. They found that the microplastics caused oxidative stress, reduced antioxidant defenses, and triggered apoptosis in the vascular cells. The study suggests that microplastics circulating in the bloodstream at realistic concentrations may contribute to vascular damage by impairing cellular protective mechanisms.
Polystyrene microplastic particles induce endothelial activation
Researchers found that polystyrene microplastic particles triggered inflammatory activation in endothelial cells lining blood vessels, increasing adhesion molecule expression and promoting leukocyte attachment. In mice, microplastic exposure led to elevated inflammatory cytokine and adhesion molecule expression in the aorta. The study identifies microplastics as a potential new environmental risk factor for vascular inflammation.
Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism
Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
Nanoplastics as emerging cardiovascular hazards: a narrative review of current evidence
This review examines the emerging evidence that nanoplastics may pose risks to cardiovascular health. Researchers summarized studies showing that nanoplastics can enter the bloodstream through ingestion, inhalation, and skin contact, potentially causing inflammation and oxidative damage to blood vessels and heart tissue. The study suggests that nanoplastic exposure represents an understudied but potentially significant environmental risk factor for heart and vascular problems.
Micro-nanoplastics and cardiovascular diseases: evidence and perspectives
Growing evidence suggests that micro- and nanoplastic particles may be a previously unrecognized risk factor for heart disease, as they have been detected in atherosclerotic plaques, heart tissue, and blood clots in humans. Lab studies show these particles can trigger oxidative stress, promote blood clotting, and cause inflammation in blood vessel cells, and their presence in artery plaques has been linked to higher rates of cardiovascular events.
Anionic nanoplastic exposure induces endothelial leakiness
Researchers discovered that nanoplastics made of anionic polystyrene and poly(methyl methacrylate) can disrupt the junctions between blood vessel cells, causing increased vascular leakiness. This effect was dose-dependent and driven by biophysical interactions rather than typical cell toxicity like oxidative stress or cell death. The findings reveal a previously unknown way that nanoplastics could affect the body's circulatory system by making blood vessels more permeable.
Stress Response of Mouse Embryonic Fibroblasts Exposed to Polystyrene Nanoplastics
Mouse embryonic fibroblasts exposed to polystyrene nanoplastics internalized particles via endocytosis without losing viability, but showed activation of antioxidant and autophagic stress pathways, suggesting subcellular dysfunction even in the absence of cell death.
Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells
Researchers found that amino-functionalized polystyrene nanoplastics can damage mitochondria in human umbilical vein endothelial cells, which line blood vessels. The study suggests that nanoplastics small enough to enter the body through the food chain may pose risks to the cardiovascular system by disrupting cellular energy production and triggering oxidative stress in vascular cells.
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.
Intrinsic Peroxidase-like Activity of Polystyrene Nanoplastics Mediates Oxidative Stress
Scientists discovered that polystyrene nanoplastics have a built-in enzyme-like ability to generate harmful reactive oxygen species, similar to how the body's own peroxidase enzymes work. This activity increased with the nanoplastics' size and aromatic chemical structure. The finding provides a new explanation for why nanoplastics cause oxidative stress in living things, which is a key mechanism behind potential health damage from plastic particle exposure.
Molecular toxicity of nanoplastics involving in oxidative stress and desoxyribonucleic acid damage
This review examines the molecular mechanisms by which nanoplastics induce oxidative stress and DNA damage in biological systems, synthesizing findings from cell culture and animal studies. The evidence suggests that nanoplastics can cause genotoxic effects at the cellular level, which is relevant to understanding potential long-term health risks of chronic nanoplastic exposure.
Co-exposure to polystyrene nanoplastics and F-53B induces vascular endothelial cell pyroptosis through the NF-κB/NLRP3 pathway
Researchers found that combined exposure to nanoplastics and a common industrial chemical (F-53B, a PFOS replacement) caused significant blood vessel damage in mice. The combination thickened artery walls, reduced blood vessel elasticity, and triggered cell death in the vessel lining through an inflammatory pathway. This suggests that nanoplastics may worsen the cardiovascular harm caused by other environmental pollutants people are commonly exposed to.
Nanoplastic-induced vascular endothelial injury and coagulation dysfunction in mice
Researchers exposed mice to polystyrene nanoplastics with different surface modifications and found that the particles caused structural damage to vascular endothelial cells and triggered inflammatory responses. The nanoplastics also disrupted blood coagulation function in the mice. The study suggests that nanoplastic exposure may pose risks to cardiovascular health due to the particles' ability to travel through the bloodstream and damage blood vessel linings.
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.
Nanoplastics exposure induces vascular malformation by interfering with the VEGFA/VEGFR pathway in zebrafish (Danio rerio)
Researchers found that nanoplastics exposure causes vascular malformation in zebrafish embryos by disrupting the VEGFA/VEGFR signaling pathway, providing new insight into how plastic nanoparticles can impair cardiovascular development.
Toxicity Induced by Micro-and Nanoplastics through Oxidative Stress: The Role of Co-Exposure to Other Chemical Pollutants
This review examined how micro- and nanoplastics cause oxidative stress — a form of cellular damage — in living organisms, particularly when combined with other chemical pollutants in the environment. Co-exposure to microplastics and chemicals like pesticides or heavy metals tends to be more damaging than either pollutant alone.
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.
Nanoplastics trigger the aging and inflammation of porcine kidney cells
Researchers exposed pig kidney cells to nanoplastics in the laboratory and found that the particles were absorbed into cells in a time- and dose-dependent manner. The nanoplastics triggered oxidative stress, leading to a buildup of reactive oxygen species in mitochondria, which in turn caused inflammatory responses and premature cell aging. The findings provide new evidence that nanoplastic exposure may contribute to kidney cell damage through oxidative stress pathways.
Micro-nanoplastic induced cardiovascular disease and dysfunction: a scoping review
This scoping review examined evidence linking micro- and nanoplastic exposure to cardiovascular disease and dysfunction, summarizing findings from animal and in vitro studies and identifying plausible mechanisms including inflammation and oxidative stress.
Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors
Researchers reviewed how nanomaterials — tiny engineered particles including nanoplastics — can trigger or worsen atherosclerosis, the buildup of fatty plaques in arteries that leads to heart attacks and strokes. The review found that nanomaterials can damage the cells lining blood vessels and provoke chronic inflammation, raising concerns about the cardiovascular risks of widespread nanomaterial exposure.
Nanoparticle-Biological Interactions in a Marine Benthic Foraminifer
Researchers exposed single-celled marine organisms called foraminifera to three types of engineered nanoparticles — including polystyrene nanoplastics — and found that all three accumulated inside the cells and triggered oxidative stress (a form of cellular damage). This study shows that even microscopic seafloor organisms are vulnerable to nanoplastic pollution, expanding the known range of species harmed by plastic contamination.
Micro- and nanoplastics: A new cardiovascular risk factor?
This review examines the growing evidence that micro- and nanoplastics may pose risks to the heart and blood vessels. Studies in animals and cell cultures show that these tiny plastic particles can enter the bloodstream, trigger inflammation, promote blood clotting, and damage blood vessel walls. While human data is still limited, the review suggests that micro- and nanoplastic exposure should be considered a potential new risk factor for cardiovascular disease.
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.