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61,005 resultsShowing papers similar to Polystyrene nanoplastics induce cardiotoxicity by upregulating HIPK2 and activating the P53 and TGF-β1/Smad3 pathways
ClearPolystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
Researchers found that polystyrene nanoplastics worsened heart damage in mice already exposed to bacterial toxins, accelerating scarring and disrupting normal heart tissue maintenance. The combined exposure triggered increased oxidative stress and activated a specific signaling pathway linked to tissue fibrosis. The study suggests that nanoplastic exposure could amplify existing cardiac stress, potentially compounding heart problems when the body is already under inflammatory challenge.
Cardiotoxicity of polystyrene nanoplastics and associated mechanism of myocardial cell injury in mice
Mice exposed to polystyrene nanoplastics for 42 days developed enlarged hearts, thinner heart walls, and weaker heart contractions in a dose-dependent manner. The nanoplastics triggered inflammation and oxidative stress in heart muscle cells through specific signaling pathways. These findings suggest that nanoplastic exposure could contribute to heart disease, including a condition called dilated cardiomyopathy.
Airborne polystyrene nanoplastics exposure leads to heart failure via ECM-receptor interaction and PI3K/AKT/BCL-2 pathways
Mice exposed to airborne polystyrene nanoplastics for just two weeks showed significant heart damage, including reduced heart mass, slowed heart rate, and signs of heart failure. The study suggests that inhaled nanoplastics harm cardiac tissue through specific molecular pathways, raising concerns about the cardiovascular risks of breathing in plastic-contaminated air.
Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats
Researchers exposed rats to polystyrene microplastics at varying concentrations for 90 days and examined cardiovascular effects. The study found that microplastic exposure activated the Wnt/beta-catenin signaling pathway and promoted cardiomyocyte apoptosis, leading to cardiac fibrosis, suggesting that chronic microplastic exposure may pose risks to cardiovascular health.
Polystyrene nanoplastics exert cardiotoxicity through the Notch and Wnt pathways in zebrafish (Danio rerio)
Researchers exposed zebrafish embryos to polystyrene nanoplastics and found dose-dependent cardiac developmental defects linked to disruption of the Notch and Wnt signaling pathways — key regulators of heart development — alongside oxidative stress, endoplasmic reticulum stress, and reduced mitochondrial activity.
Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
Researchers exposed mice to polystyrene nanoplastics through inhalation and found that even short-term breathing exposure caused heart damage, including inflammation and weakened heart function. The damage got worse with higher doses and longer exposure times, with energy production in heart cells being disrupted through mitochondrial damage. This is one of the first studies to show that breathing in nanoplastics can directly harm the heart, raising concerns about airborne plastic particle exposure in humans.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
Embryonic exposure of polystyrene nanoplastics affects cardiac development
Researchers found that polystyrene nanoplastics disrupted the development of heart cells grown from human embryonic stem cells, producing smaller and weaker heart tissue in the lab. The nanoplastics caused oxidative stress in mitochondria and blocked important cellular cleanup processes, reducing the stem cells' ability to properly form heart cells. In zebrafish embryos, nanoplastic exposure also reduced heart contractions and blood flow, suggesting that nanoplastic exposure during pregnancy could pose risks to fetal heart development.
Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice
Long-term exposure to tiny polystyrene nanoplastics caused atherosclerosis (hardening of the arteries) in mice by disrupting fat metabolism in the liver and triggering inflammation and oxidative stress. This is one of the first studies to directly link nanoplastic exposure to cardiovascular disease development, raising concerns about heart health risks from the nanoplastics found in our food and environment.
Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids
Researchers found that even low doses of polystyrene microplastics can damage heart tissue in both mice and lab-grown human heart organoids. The microplastics triggered oxidative stress and disrupted energy production in heart cells, leading to inflammation and cell death. This is one of the first studies to show heart-specific toxicity from microplastics at doses meant to reflect realistic human exposure levels.
Cytotoxic and dysmetabolic impact of polystyrene nanoplastics, a new potential atherosclerotic cardiovascular risk factor, on a steatosis model of HepG2 cells
Researchers exposed cell cultures to polystyrene nanoplastics and found significant cytotoxic effects and metabolic disruption including mitochondrial dysfunction and altered glucose metabolism, suggesting nanoplastics may act as a novel class of metabolic disruptors.
Evaluation of Polystyrene Nanoplastics Induced Cardiotoxicity Under Different Dietary Patterns in Mice
Researchers exposed mice fed different dietary patterns to polystyrene nanoplastics and assessed cardiac toxicity. The study found that dietary habits significantly modulated nanoplastic-induced heart damage, demonstrating that diet is an important variable in evaluating the health risks of foodborne plastic contaminants.
Unveiling the Heart’s Hidden Enemy: Dynamic Insights into Polystyrene Nanoplastic-Induced Cardiotoxicity Based on Cardiac Organoid-on-a-Chip
Using a human heart organoid-on-a-chip (a miniature lab-grown heart model), researchers tracked how polystyrene nanoplastics damage the heart over time. Short-term exposure caused oxidative stress, inflammation, and disrupted calcium signaling, while long-term exposure led to heart scarring (fibrosis). Notably, even low doses that seemed harmless in healthy tissue worsened damage in heart tissue already affected by a simulated heart attack.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes
Researchers found that polystyrene microplastics caused serious heart damage in chickens by triggering oxidative stress, inflammation, and disruption of the cells' energy production systems. The microplastics activated inflammatory pathways that led to a type of cell death called pyroptosis and damaged the mitochondria that power heart cells. These findings suggest that microplastic exposure could pose risks to cardiovascular health in animals, with potential implications for understanding heart-related effects in humans.
Toxicity of long term exposure to low dose polystyrene microplastics and nanoplastics in human iPSC-derived cardiomyocytes
Researchers exposed human heart cells grown from stem cells to very low doses of polystyrene micro- and nanoplastics over an extended period and found that the particles reduced the cells' ability to contract and disrupted their electrical signaling. The smaller nanoplastics (50 nm) caused more severe damage than the larger microplastics (1 micrometer), including increased cell death and calcium handling problems. This study provides direct evidence that even low-level microplastic exposure could harm human heart function.
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.
Mechanism of Nano‐Microplastics Exposure‐Induced Myocardial Fibrosis: DKK3‐Mediated Mitophagy Dysfunction and Pyroptosis
Researchers investigated how nano-microplastic exposure leads to heart tissue scarring in mice and identified a specific molecular pathway involved. They found that the plastic particles suppressed a protein called DKK3, which disrupted the cell's ability to recycle damaged mitochondria, triggering an inflammatory cell death process that promotes fibrosis. The study reveals a potential mechanism by which long-term microplastic exposure could contribute to cardiac damage.
Prepuberty exposure to polystyrene nanoplastics induces cardiac inflammation through calcium overload-mediated ROS/JAK1/STAT3 signaling cascade
Researchers found that exposing young rats to polystyrene nanoparticles through drinking water during prepuberty induced cardiac inflammation by triggering calcium overload in heart cell mitochondria, which then activated the ROS/JAK1/STAT3 inflammatory signaling cascade — identifying a potential developmental window of vulnerability to nanoplastic cardiovascular toxicity.
Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways
Tiny plastic particles called micro- and nanoplastics are getting into our bodies through food, air, and skin contact, and researchers have found them building up in people's hearts and blood vessels. This review of existing studies shows these plastic bits may contribute to heart disease by causing inflammation and damaging cells in the cardiovascular system. While more research is needed, this suggests that plastic pollution isn't just an environmental problem—it could be directly harming our heart health.
Exposure to polystyrene microplastics with different functional groups: Implications for blood pressure and heart
In a rat study, exposure to polystyrene microplastics raised blood pressure by 22-40% and caused heart muscle enlargement and oxidative damage, with chemically modified microplastics causing even worse effects. The research identified a molecular pathway involving reduced blood vessel-relaxing signals that may explain how microplastic exposure contributes to cardiovascular disease.
Adolescent exposure to polylactic acid microplastics causes cardiac fibrosis by promoting cardiomyocyte senescence
Adolescent mice exposed to polylactic acid (PLA) biodegradable microplastics developed cardiac fibrosis, with mechanistic studies showing that PLA particles promoted cardiomyocyte senescence and activated inflammatory signaling, demonstrating cardiotoxicity from a supposedly 'green' plastic.
Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp
Researchers exposed carp to polystyrene microplastics and found they caused heart tissue inflammation, cell death, and necrosis through activation of the TLR4/NF-kB inflammatory pathway. The damage increased with higher microplastic concentrations, with both apoptosis and necrosis observed in heart muscle cells. The study provides evidence that microplastic exposure can directly harm cardiovascular tissue in fish.