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Micro(nano)plastics in the Development of Myocardial Fibrosis: From Clinical Detection to Molecular Mechanism
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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.
BACKGROUND: Micro(nano)plastics (MNPs) are pervasive environmental contaminants, yet their presence in human cardiac tissue and their potential contribution to myocardial fibrosis remain unclear. We investigated whether myocardial MNP burden is associated with fibrosis severity in patients and evaluated mechanistic plausibility in mice. METHODS: Left atrial appendage tissues were collected from patients undergoing cardiac surgery (n=33). MNP burden and polymer composition were quantified by pyrolysis-gas chromatography/mass spectrometry, and fibrosis was quantified histologically. In mice, 100-nm or 1-µm polystyrene nanoplastics were administered by oral gavage in coexposure and sequential exposure protocols with isoprenaline. Cardiac function was assessed by echocardiography, and fibrosis was evaluated by histology and immunohistochemistry. Transcriptomics, metabolomics, and 16S ribosomal RNA sequencing were performed to identify pathways linked to MNP exposure. RESULTS: =0.002). Transcriptomics indicated activation of inflammatory and profibrotic pathways (TNF/NF-κB [nuclear factor-κB], TGF-β [transforming growth factor-beta], and MAPK), supported by increased α-SMA (alpha-smooth muscle actin), COL1 (collagen I), and TGF-β1 immunostaining, while metabolomics suggested perturbations in lipid metabolism and mitochondrial function. In mice, polystyrene exposure exacerbated isoprenaline-induced systolic dysfunction and myocardial fibrosis in both experimental paradigms and recapitulated pathway signatures related to cell-matrix interactions. CONCLUSIONS: Myocardial MNP burden, particularly nanoplastics, is associated with greater fibrosis in humans, and experimental polystyrene exposure aggravates stress-induced myocardial remodeling in vivo. Multiomics analyses nominate inflammatory, ECM (extracellular matrix), and metabolic programs as candidate mediators of MNP-associated cardiotoxicity.
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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.
Environmental Pollutant–Induced Cardiopathogenesis Through Immune Dysfunction: The Emerging Role of Micro- and Nanoplastics
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Researchers reviewed experimental and clinical evidence linking micro- and nanoplastic exposure to cardiovascular disease, showing that MNPs detected in human vascular and cardiac tissues promote macrophage inflammation, disrupt endothelial barriers, activate NLRP3 inflammasome signaling, and amplify oxidative stress — converging mechanisms that increase vulnerability to atherosclerosis, arrhythmia, and ischemic injury.
Polystyrene nanoplastics induce cardiotoxicity by upregulating HIPK2 and activating the P53 and TGF-β1/Smad3 pathways
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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.
Cardiotoxicity of polystyrene nanoplastics and associated mechanism of myocardial cell injury in mice
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Mice exposed to polystyrene nanoplastics for 42 days developed enlarged hearts, thinner heart walls, and weaker heart contractions in a dose-dependent manner. The nanoplastics triggered inflammation and oxidative stress in heart muscle cells through specific signaling pathways. These findings suggest that nanoplastic exposure could contribute to heart disease, including a condition called dilated cardiomyopathy.
Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats
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Researchers exposed rats to polystyrene microplastics at varying concentrations for 90 days and examined cardiovascular effects. The study found that microplastic exposure activated the Wnt/beta-catenin signaling pathway and promoted cardiomyocyte apoptosis, leading to cardiac fibrosis, suggesting that chronic microplastic exposure may pose risks to cardiovascular health.
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