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Inhibition of AMPK Signaling Pathway Mediates Cardiotoxicity Induced by Co-Exposure to Polylactic Acid Nanoplastics and Silica Nanoparticles
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Scientists found that two types of tiny particles common in food packaging and processed foods—plastic nanoparticles (from biodegradable plastics) and silica nanoparticles (a common food additive)—caused more heart damage in mice when combined than either did alone. The combo disrupted a key cellular energy-regulating system, leading to stressed mitochondria (the cell's power plants) and heart cell death. While this study was done in mice, it raises concerns that everyday combinations of food-related nanoparticles might pose greater risks to heart health than scientists previously realized from studying them separately.
Emerging evidence suggests that synergistic toxic effects are induced upon co-exposure to different food contaminants. Considering that polylactic acid nanoplastics (PLA-NPLs) and synthetic amorphous silica (SAS) are widely used in food industry, it is of great importance to investigate whether the nano-scale derivatives, PLA-NPLs and silica nanoparticles (SiNPs), would exhibit synergistic cardiotoxic effects. Here, we investigated the synergistic cardiotoxic effects of PLA-NPLs and SiNPs in male C57BL/6J mice. The results revealed that compared with single exposure,co-exposure to PLA-NPLs and SiNPs would significantly aggravate cardiotoxicity probably by inducing cardiac contractile dysfunction and remodeling. This cardiotoxicity was associated with inhibition of the Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway, which impaired mitochondrial homeostasis, induced oxidative stress, and ultimately triggered cardiomyocyte apoptosis. Meanwhile, the AMPK activator Metformin and the mitochondria targeted Reactive Oxygen Species (ROS) scavenger Mito-TEMPO were further used to confirm the involvement of AMPK signaling and ROS. In summary, co-exposure to PLA-NPLs and SiNPs would induce more severe cardiac injury and provide mechanistic insights for the synergistic toxicity of food contaminants in mammalian systems.
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Polystyrene nanoplastics and cadmium co-exposure aggravated cardiomyocyte damage in mice by regulating PANoptosis pathway
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Researchers gave mice low doses of polystyrene nanoplastics and cadmium (a toxic metal) together and found that the combination caused significantly worse heart damage than either substance alone. The damage involved a newly recognized form of cell death called PANoptosis, which combines multiple destructive pathways in heart cells. This suggests that real-world exposure to nanoplastics alongside common environmental pollutants like cadmium could compound risks to heart health.
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.
Polystyrene nanoplastics induce cardiotoxicity by driving myocardial metabolic reprogramming via the SDHA/Succinate/HIF-1α axis
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Scientists found that tiny plastic particles (nanoplastics) can damage heart cells by messing with how they produce energy, forcing them to rely on a less efficient "backup" fuel system instead of their normal one. This energy imbalance triggers a chain reaction inside heart cells that weakens their ability to contract properly, which was confirmed in mice, human heart cells, and lab-grown human heart tissue. While this research was done in animal and cell models rather than humans directly, it adds to growing evidence that the microplastics we're constantly exposed to in food, water, and air may pose real risks to heart health.
Polystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
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Researchers found that polystyrene nanoplastics worsened heart damage in mice already exposed to bacterial toxins, accelerating scarring and disrupting normal heart tissue maintenance. The combined exposure triggered increased oxidative stress and activated a specific signaling pathway linked to tissue fibrosis. The study suggests that nanoplastic exposure could amplify existing cardiac stress, potentially compounding heart problems when the body is already under inflammatory challenge.
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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