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Adolescent exposure to polylactic acid microplastics causes cardiac fibrosis by promoting cardiomyocyte senescence
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Adolescent mice exposed to polylactic acid (PLA) biodegradable microplastics developed cardiac fibrosis, with mechanistic studies showing that PLA particles promoted cardiomyocyte senescence and activated inflammatory signaling, demonstrating cardiotoxicity from a supposedly 'green' plastic.
Population studies and animal experiments have indicated that exposure to microplastics (MPs) is closely related to adverse cardiovascular outcomes. However, as far as we know, all current studies on MPs-induced cardiotoxicity are limited to traditional petroleum-based plastics, and there is a blank for potential heart damage caused by 'bioplastics' made of polylactic acid (PLA) materials. This study investigated the cardiotoxicity of PLA-MPs in mice and its potential mechanism. Adolescent mice exposed to PLA-MPs for 28 days showed obvious cardiac developmental toxicity, manifested as disordered arrangement of myocardial cells, thinning of myocardial thickness and fibrosis. Further studies found that ferroptosis and senescence were observed in the hearts of adolescent mice exposed to PLA-MPs. In vitro, we used H9c2 cells to study the cellular internalization, senescence and ferroptosis effects of PLA-MPs. We found that PLA-MPs exposure increased the senescence characteristics of H9c2 cells, such as increased SA-β-Gal activity, up-regulated expression of senescence-associated proteins (p16, p21, γH2AX) and senescence-associated inflammatory factors. Moreover, we found that PLA-MPs caused ferroptosis in H9c2 cells with elevated ferrous iron. Subsequent studies found that Fer-1 inhibited ferroptosis signal and alleviated PLA-MPs-induced H9c2 cell senescence. In summary, our findings highlight the cardiotoxic effects of biodegradable PLA-MPs through ferroptosis and senescence pathways, and provide insights into the toxicological effects of biodegradable MPs on mammalian cardiovascular system capacity.
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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.
Aged polylactic acid microplastics exacerbate lipid metabolism disorders and cardiac dysfunction via PPARγ activation in zebrafish: A comparative study with polymers and oligomers
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Researchers compared the toxicity of polylactic acid microplastics at different degradation stages—polymers, oligomers, and aged polymers—in zebrafish larvae, finding that aged PLA most severely disrupted lipid metabolism and cardiac function through PPARγ activation.
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.
Nanoplastics causes heart aging/myocardial cell senescence through the Ca2+/mtDNA/cGAS-STING signaling cascade
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Researchers discovered that nanoplastics can cause heart aging by entering heart muscle cells and triggering a chain reaction: they damage mitochondria (the cell's energy source), which leaks DNA into the cell, activating an immune alarm system called the cGAS-STING pathway. This is the first study to reveal how long-term nanoplastic exposure could accelerate heart aging, raising concerns about the cardiovascular effects of plastic pollution.
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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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.