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Polystyrene Nanoplastics Induce Pyroptosis in HepG2 Cells via the YAP1-cGAS-STING Signaling Axis.
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Scientists found that tiny plastic particles from polystyrene (commonly used in disposable cups and food containers) can trigger a harmful type of cell death in liver cells. When these microscopic plastic pieces enter liver cells, they activate a specific pathway that causes the cells to essentially self-destruct, which could potentially damage the liver over time. This research helps explain how the plastic pollution we're exposed to daily might be harming our bodies, particularly our liver health.
These findings indicate that PS-NPs promote hepatocyte pyroptosis through the YAP1-cGAS-STING pathway, with YAP1 serving as a central regulator, providing mechanistic insight into PS-NPs-induced liver toxicity and identifying YAP1 as a potential therapeutic target.
More Papers Like This
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway
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Researchers found that tiny polystyrene microplastics (0.1 micrometers) can enter liver cells and cause DNA damage that triggers a chain reaction leading to liver scarring, known as fibrosis. The microplastics activated a specific immune signaling pathway called cGAS/STING, which caused inflammation that progressively damaged liver tissue even at low concentrations. This study reveals a specific mechanism by which long-term microplastic exposure could lead to serious liver disease in humans.
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
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Researchers discovered that very small polystyrene nanoparticles (20 nanometers) cause liver damage in mice by accumulating inside immune cells called macrophages, disrupting their energy-producing structures (mitochondria), and triggering a form of cell death that then spreads damage to liver cells. This study reveals a specific mechanism by which nanoplastic exposure could harm the liver, an organ critical for filtering toxins from the body.
Polystyrene microplastic exposure induces hepatic damage via immune-modulated autophagy and ferroptosis in Nile tilapia (Oreochromis niloticus)
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Scientists found that tiny plastic particles (microplastics) can damage the liver in fish by triggering inflammation and a type of cell death linked to iron and fat breakdown, essentially causing cells to self-destruct in a harmful way. While this study was done in tilapia, not humans, it adds to growing evidence that the microplastics we're increasingly exposed to through food, water, and air may cause similar organ damage in other animals—including potentially us—making this an important area for future human health research.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.