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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.
Micro- and nano-plastics (MNPs) have emerged as ubiquitous environmental contaminants and are increasingly implicated in adverse cardiovascular outcomes, yet their induced cardiotoxicity and potential mechanisms remain poorly understood. This study integrated in vivo mouse models, AC16 cardiomyocytes and a human cardiac organoid-on-a-chip (COoC) platform to multi-dimensionally evaluate polystyrene nanoparticles (PS-NPs)-induced cardiac injury and clarify its key molecular mechanisms. We found that PS-NPs exposure induced pronounced structural and functional cardiac injury in mice and caused impaired myocardial contraction, disrupted calcium transients and increased injury biomarkers in vitro . Notably, PS-NPs exposure perturbed myocardial energy metabolism, producing a metabolic reprogramming profile characterized by suppressed fatty acid oxidation (FAO) and enhanced glycolytic activity. Metabolic interventions further showed that activation of FAO or promotion of mitochondrial pyruvate oxidation improved myocardial energy status and alleviated cardiotoxicity, whereas direct inhibition of glycolysis aggravated energy depletion and cellular injury, suggesting that enhanced glycolysis provided partial energetic compensation but was insufficient to offset impaired oxidative metabolism. Mechanistically, our findings indicated a functional role of the SDHA/succinate/HIF-1α signaling axis in this metabolic reprogramming. PS-NPs-induced SDHA downregulation promoted succinate accumulation and HIF-1α stabilization, thereby rewiring myocardial energy metabolism and contributing to cardiac dysfunction. Collectively, we revealed myocardial metabolic reprogramming as an important mechanism underlying PS-NPs-induced cardiotoxicity and identified the SDHA/succinate/HIF-1α axis as a potential molecular link between PS-NPs exposure and cardiac injury.
More Papers Like This
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.
Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids
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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.
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.
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.
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.
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