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Propionic acid/FBP1 is involved in polystyrene nanoplastic-induced cardiac injury via the gut-heart axis
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Researchers found that polystyrene nanoplastic exposure in animals reduced levels of a gut-produced fatty acid called propionic acid, which in turn suppressed a heart-protective protein (FBP1) and led to cardiac injury — revealing a gut-to-heart pathway by which nanoplastic exposure may damage cardiovascular health.
In summary, our study systematically demonstrated the role of gut-heart axis in NPs-induced cardiac injury, and the specific process was that NPs exposure reduced propionate level, which in turn inhibited FBP1 expression to impair cardiac function. These findings provide new insights into NPs-induced cardiotoxicity and identifie potential therapeutic targets, providing clues for the prevention and treatment of NPs-induced cardiac injury in the future.
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Researchers found that micro- and nanoplastic burden in human cardiac tissue—particularly nanoplastics—was positively associated with myocardial fibrosis severity, and confirmed in mice that polystyrene nanoplastic exposure worsens stress-induced cardiac remodeling by activating inflammatory, extracellular matrix, and metabolic pathways.
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Researchers exposed mice fed different dietary patterns to polystyrene nanoplastics and assessed cardiac toxicity. The study found that dietary habits significantly modulated nanoplastic-induced heart damage, demonstrating that diet is an important variable in evaluating the health risks of foodborne plastic contaminants.
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Researchers found that polystyrene nanoplastics disrupt the gut lining in mice by altering tiny RNA molecules that control the production of protective proteins in the intestinal barrier. The nanoplastics also caused an imbalance in gut bacteria, creating a chain reaction where damaged gut cells release particles that further weaken the intestinal barrier and change the microbiome.
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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.
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Researchers demonstrated that oral exposure to polystyrene nanoplastics in mice causes cardiac fibrosis, cardiomyocyte death, and impaired heart function by upregulating the protein HIPK2 and activating P53 and TGF-β1/Smad3 signaling pathways, with effects worsened in animals with pre-existing heart disease — implicating nanoplastics as a cardiovascular risk factor.
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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.