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61,005 resultsShowing papers similar to Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
ClearDissection 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.
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.
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.
PVC nanoplastics impair cardiac function via lysosomal and mitochondrial dysfunction
Researchers found that PVC nanoplastics damaged heart cells by disrupting two critical cellular structures: lysosomes (the cell's recycling system) and mitochondria (the cell's energy producers). The nanoplastics caused lysosomes to become leaky and mitochondria to malfunction, leading to heart cell injury and impaired cardiac function. This study is concerning because PVC is one of the most common plastics, and the findings suggest that nanoplastic exposure could contribute to heart disease.
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.
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.
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.
Influence of Micro- and Nanoplastics on Mitochondrial Function in the Cardiovascular System: A Review of the Current Literature
This review examined the limited but growing research on how micro- and nanoplastics may affect mitochondrial function in the cardiovascular system. Researchers noted that these plastic particles can trigger oxidative stress and disrupt normal mitochondrial processes, which are critical for heart and blood vessel health. The study highlights the need for more comprehensive research given the rising levels of plastic particle contamination and the importance of mitochondrial health in preventing cardiovascular problems.
Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells
Researchers exposed normal human liver and lung cells to 80-nanometer plastic particles and found that the nanoplastics damaged mitochondria, the energy-producing structures inside cells, without causing widespread cell death. Using metabolomics analysis, they identified specific disruptions to energy metabolism and lipid processing pathways in both cell types. This study reveals a subtle but important way that nanoplastics could impair organ function in humans by disrupting cellular energy production.
Nanoplastics causes heart aging/myocardial cell senescence through the Ca2+/mtDNA/cGAS-STING signaling cascade
Researchers discovered that nanoplastics can cause heart aging by entering heart muscle cells and triggering a chain reaction: they damage mitochondria (the cell's energy source), which leaks DNA into the cell, activating an immune alarm system called the cGAS-STING pathway. This is the first study to reveal how long-term nanoplastic exposure could accelerate heart aging, raising concerns about the cardiovascular effects of plastic pollution.
Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis
Researchers reviewed evidence that micro- and nanoplastics detected in human cardiovascular tissues may contribute to cardiovascular disease through mitochondrial dysfunction. The study found that these particles can impair mitochondrial integrity, induce oxidative stress, disrupt calcium signaling, and promote genomic instability, suggesting a mechanistic link between plastic particle exposure and cardiovascular pathology.
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.
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.
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.
Unveiling the underlying mechanism: Metabolic reprogramming and oxidative stress mediate nanoplastic-induced hepatotoxicity in a freshwater fish (Pseudorasbora parva)
Scientists studied how tiny plastic particles (nanoplastics) affect fish livers and found that the smallest particles (80 nanometers) caused the most damage by disrupting the body's ability to fight harmful chemicals and process energy. The smallest plastic particles were especially harmful because they damaged the fish's natural defense systems and changed how their cells make energy. While this study was done in fish, it raises concerns about how these tiny plastic particles in our environment might also harm human 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.
Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases
This review summarizes how nanoplastics, which are small enough to enter individual cells, damage mitochondria (the energy-producing structures inside cells) by disrupting their shape, function, and ability to produce energy. This mitochondrial damage has been linked to a range of diseases including neurodegeneration, diabetes, cardiovascular disease, and reproductive problems. The findings help explain why nanoplastic exposure may contribute to multiple chronic health conditions through a common cellular mechanism.
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.
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.
Impact of Micro- and Nanoplastics on Mitochondria
This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
Cellular Distribution of Polystyrene Nanoplastics from Food Chain and Their Effects on Mitochondrial Quality in H9C2 Cells
Researchers investigated the cellular distribution of polystyrene nanoplastics entering via the food chain and examined their effects on mitochondrial quality in H9C2 cardiac cells, assessing how nanoplastic accumulation disrupts mitochondrial function.
Polystyrene nanoplastics induced cardiomyocyte apoptosis and myocardial inflammation in carp by promoting ROS production
Researchers exposed carp to polystyrene nanoplastics of different sizes and found that the particles caused heart muscle cell death and cardiac inflammation. Smaller nanoplastics penetrated deeper into heart tissue and caused more severe damage by promoting the production of reactive oxygen species. The study provides evidence that nanoplastic pollution in aquatic environments can directly harm fish 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.