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Nanoplastics induces arrhythmia in human stem-cells derived cardiomyocytes
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Researchers exposed human cardiomyocytes derived from stem cells to nanoplastic particles and observed dose-dependent uptake, oxidative stress, and arrhythmias developing by day seven. Complementary experiments in mice revealed that nanoplastics disrupted RNA processing and protein folding in heart tissue, leading to cellular stress and impaired electrical signaling. The study provides evidence that nanoplastic exposure may pose direct risks to heart rhythm and function.
Nanoplastics (NPs), plastic particles ranging from 1-1000 nm, form through weathering and are considered more hazardous than larger plastics due to their ability to penetrate cell barriers and be internalised by biological systems. Most research on NPs has focused on animal models, examining effects on the brain, lungs, and gastrointestinal tract. To enhance physiological relevance, this study investigated the impact of NPs on human cardiomyocytes (CMs) derived from human embryonic stem cells (hESCs). We observed significantly higher cellular uptake of 50 nm NPs compared to 500 nm particles, with dose-dependent accumulation over 3, 5, and 7 days of treatment. This accumulation induced oxidative and endoplasmic reticulum (ER) stress, culminating in arrhythmias by day 7. Complementing these in vitro findings, transcriptome profiling of mice exposed to NPs for 8 weeks revealed disrupted RNA splicing, dysregulated protein translation, and defective protein folding. These molecular changes led to ER stress, apoptosis, and impaired transmembrane ion conductance, contributing to the arrhythmic phenotype. Our findings highlight the detrimental effects of NPs on the human heart. Further research is needed to fully elucidate the mechanisms underlying NP-induced toxicity and to develop strategies for mitigating their adverse effects. This study underscores the urgency of addressing NP pollution to protect human health.
More Papers Like This
Nanoplastics induces Arrhythmia in Human Stem-cells derived Cardiomyocytes
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Exposing human embryonic stem cell-derived heart muscle cells to nanoplastics for up to seven days caused dose-dependent oxidative stress, increased cell death, and — by day seven — abnormal electrical activity consistent with cardiac arrhythmia. These findings provide the first direct evidence using human heart cells that nanoplastic accumulation can disrupt cardiac function, raising important questions about long-term cardiovascular risks from plastic particle exposure in people.
Embryonic exposure of polystyrene nanoplastics affects cardiac development
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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.
Toxicity of long term exposure to low dose polystyrene microplastics and nanoplastics in human iPSC-derived cardiomyocytes
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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.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
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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.
Exposure to nanoplastics impairs collective contractility of neonatal cardiomyocytes under electrical synchronization
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Researchers studied how nanoplastics affect the contraction of neonatal rat heart cells in the lab. They found that positively charged nanoplastics accumulated on cell membranes and entered cells, leading to reduced calcium levels, disrupted electrical activity, mitochondrial damage, and increased reactive oxygen species, ultimately impairing the heart cells' ability to contract.
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