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PVC nanoplastics impair cardiac function via lysosomal and mitochondrial dysfunction
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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.
MICRO: and nanoplastics (MNPs) are emerging environmental pollutants that pose a significant threat to human health, with traces found in cardiac tissues. While previous studies have indicated that MNPs can cantribute to cardiac dysfunction, there is limited systematic investigation into how MNPs exposure affects various organelles. This study focuses on polyvinyl chloride nanoparticles (PVC NPs), one of the most common and persistent plastic pollutants in the environment. Our findings reveal that PVC NPs engage in organelle-specific interactions, predominantly accumulating in the lysosomes and mitochondria of cardiomyocytes. This targeted accumulation results in substantial disruptions to lysosomal autophagic flux and mitochondrial energy metabolism. These results offer new insights into the organelle-specific mechanisms behind PVC NP-induced cardiotoxicity, highlighting the distinct risks associated with this widespread environmental contaminant.
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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.
Polymer-specific nanoplastic exposure, mitochondrial dysfunction, and depressed ejection fraction in humans.
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In older adults, higher blood levels of two plastic particle types, polystyrene and polyethylene, were linked to weaker heart pumping function. In lab tests on human heart muscle cells, these particles built up inside cells and disrupted their energy-producing structures, with each type causing a different pattern of damage.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
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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 Nanoplastics Induce Early Mitochondrial Dysfunction in H9c2 Cardiomyoblasts Without Substantial Cell Damage
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Scientists exposed heart muscle cells to nanoplastics (tiny plastic particles similar to those found in human blood and heart tissue) and found that even without killing the cells or causing obvious damage, the plastics quietly disrupted the cells' mitochondria — the "power plants" that generate energy. This means the heart cells' ability to produce extra energy during stress or exertion may be weakened, even though everything looks normal on the surface. While this was a lab study on cells (not people), it raises concern that everyday plastic exposure could be subtly straining our hearts' energy reserves over time.
Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
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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.
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