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61,005 resultsShowing papers similar to Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids
ClearToxicity 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.
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.
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.
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.
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.
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.
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.
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.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
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.
The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis
A rat study using metabolomics analysis found that long-term exposure to high concentrations of polystyrene microplastics led to abnormal fat metabolism and cardiovascular damage. The harm appeared to be driven by oxidative stress and inflammation, suggesting that chronic microplastic exposure could contribute to heart and blood vessel disease.
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.
Changes in Cardiovascular Structure and Physiology Following Polystyrene Nanoparticle Exposure
This review examines how polystyrene microplastics can harm the cardiovascular system, which is among the first organs exposed after particles enter the body through ingestion or inhalation. Evidence suggests microplastics may cause structural and physiological changes to the heart and blood vessels, highlighting the need for more research into this risk.
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.
Cardiotoxicity of Microplastics: An Emerging Cardiovascular Risk Factor
This review examines emerging evidence that microplastics may pose risks to cardiovascular health, summarizing findings from laboratory and animal studies. Researchers found that microplastic exposure has been linked to inflammation, oxidative stress, and disrupted heart function in experimental settings. Given that cardiovascular disease is already the leading cause of death globally, the study suggests that microplastics as a potential contributing factor warrant urgent further investigation.
Effects of polystyrene microplastics on mice cardiac tissue structure: Protective role of resveratrol
Researchers exposed mice to polystyrene microplastics for 90 days and found that the particles caused significant oxidative stress and structural damage to heart tissue. However, when mice also received resveratrol, a natural antioxidant compound found in grapes and berries, much of the cardiac damage was prevented. The study suggests that antioxidant compounds may offer some protective benefit against microplastic-induced heart tissue damage.
Adverse effects polystyrene microplastics exert on zebrafish heart – Molecular to individual level
Researchers fed zebrafish microplastic-enriched food for 21 days and found significant damage to heart function, including reduced contraction strength and frequency, along with decreased swimming ability. At the cellular level, the fish showed increased oxidative stress, DNA damage, and disrupted energy metabolism in heart tissue. The study provides evidence that microplastic exposure can affect cardiovascular health in fish from the molecular level up to whole-organism fitness.
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.
Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice
Researchers fed mice polystyrene microplastic beads and found that ingestion promoted fat accumulation and markers of cardiometabolic disease, including changes in cholesterol levels and inflammatory markers. The microplastics appeared to disrupt metabolic processes related to fat storage and energy regulation. The study suggests that dietary microplastic exposure may contribute to obesity and cardiovascular risk factors, adding a new dimension to concerns about microplastics in the food supply.
Microplastics: A Matter of the Heart (and Vascular System)
This review summarizes growing evidence that microplastics and nanoplastics can damage the heart and blood vessel system in both fish and mammals. In fish, plastic particles enter through the gills and trigger inflammation, disrupt blood chemistry, promote blood clots, and cause heart damage. In mammals, including humans, microplastics interact with blood cells and proteins, travel to the heart, and cause oxidative stress in heart muscle cells, raising concerns about long-term cardiovascular health effects.
Impacts of micro- and nanoplastic exposure on the cardiovascular system: a systematic review focused on in vivo studies
This systematic review summarizes 38 animal studies on how micro- and nanoplastics affect the heart and blood vessels. The research found that these tiny plastic particles can deposit in cardiovascular tissue, trigger inflammation and oxidative stress, and cause structural damage, raising concerns about potential heart health risks from ongoing plastic exposure.
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.
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.