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Cardiotoxic Effect Induced by F-53B via Nitric Oxide Signalling on Parkin−/− Mice
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Researchers investigated how the emerging PFAS compound F-53B affects cardiac health in mice lacking the parkin gene, finding that exposure caused significant cardiac fibrosis (up to 2.8-fold increase) and suppressed the eNOS/nitric oxide signaling pathway critical for vascular function. These results demonstrate that PFAS can cause cardiotoxicity even at environmentally relevant doses, with gene-environment interactions amplifying the damage.
A comprehensive understanding of gene-environment interactions is essential for maintaining human cardiac health, and deficiency in the key parkin gene exacerbates cardiac injury. Per- and polyfluoroalkyl substances (PFAS) exposure has been determined cardiotoxicity from the epidemiological perspective but the potential remained unclear. Here, we investigated the co-effects on cardiac pathological structure and function of an emerging PFAS, 6:2 chlorinated polyfluorinated ether sulfonate acid (F-53B), on male parkin-/- mice at dose of 3 and 3000 μg/kg for 60 d. Mechanism was focused on the activity, phosphorylation of endothelial nitric oxide synthase (eNOS), and the content of nitric oxide (NO), vital vascular function regulating molecule. F-53B significantly increased cardiac fibrosis to 1.58- and 2.80-fold, and cardiac troponin T (cTNT) to 1.17- and 1.32-fold compared with control group, at dose of 3 and 3000 μg/kg, respectively, indicating F-53B can inhibit the normal activities of the heart and cause functional disorders. Content and phosphorylation of eNOS significantly decreased to 0.68-, 0.67-fold, and to 0.65-, 0.54-fold compared with control group, respectively. The subsequent content of NO level was also significantly decreased to 0.47- and 0.33-fold, respectively, indicating that significant co-effects of parkin deficiency and F-53B exposure on cardiac function and structural changes via eNOS/NO signalling. Our work underscores the importance of assessing cardiac risk associated with PFAS at environmentally relevant doses, especially considering environmental exposure and gene co-interaction from the perspective of F-53B and parkin gene.
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Researchers found that combined exposure to nanoplastics and a common industrial chemical (F-53B, a PFOS replacement) caused significant blood vessel damage in mice. The combination thickened artery walls, reduced blood vessel elasticity, and triggered cell death in the vessel lining through an inflammatory pathway. This suggests that nanoplastics may worsen the cardiovascular harm caused by other environmental pollutants people are commonly exposed to.
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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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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.
Co-exposure to F-53B and nanoplastics induced hepatic glucolipid metabolism disorders by the PI3K-AKT signaling pathway
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Researchers studied the combined effects of the industrial chemical F-53B and nanoplastics on liver function in mice over two months. They found that co-exposure caused liver swelling and disrupted both fat and sugar metabolism through a specific signaling pathway, with effects more severe than either substance alone. The study suggests that nanoplastics may enhance the liver toxicity of fluorinated industrial chemicals by increasing their accumulation in the body.
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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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