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Polystyrene nanoplastics promote muscle cell senescence through microtubule hyper-stabilization-mediated mitophagy dysfunction and cGAS-Sting activation
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Researchers found that polystyrene nanoplastics cause premature aging in human muscle cells by disrupting the internal skeleton of cells and impairing the cleanup of damaged mitochondria. The nanoplastics made the cell's structural framework too rigid, which blocked normal cell signaling and triggered an inflammatory aging response. This study suggests that nanoplastic exposure could contribute to muscle weakness and age-related muscle loss in humans.
The detrimental effects of polystyrene nanoplastics (NPs) on human skeletal muscle cells and underlying mechanisms remain largely unclear. Here we exposed mice to NPs and observed significant NP uptake and damages in muscles. RNA sequencing result revealed that many cytoskeleton-related factors were markedly altered by NPs. With cultured human muscle cells, we demonstrate that internalized NPs profoundly changed the microtubule network by causing increased tubulin acetylation, enhanced stabilization, and reduced dynamics. These microtubule changes were accompanied by impaired microtubule-organizing center (MTOC) functionality, defective mechanotransduction capacity linked to YAP deactivation, and critically, compromised function as trafficking tracks for intracellular organelles like mitochondria and lysosomes, leading to accumulation of damaged mitochondria and dysfunctional mitophagy at MTOC location. mtDNA leakage from damaged mitochondria then led to cGAS-Sting activation and accelerated cellular senescence. Mechanistically, NP-induced microtubule hyper-stabilization was driven by deactivation of tubulin deacetylases Sirt2 and HDAC6, leading to α-tubulin hyperacetylation. Further, Sirt2 reactivation/overexpression in muscle cells effectively reduced NP-induced α-tubulin acetylation, mitochondrial damage, cGAS-Sting activation and cellular senescence, as well as the level of cytoplasmic NPs. Our findings unveil a novel mechanism by which NPs promote cellular senescence, highlighting microtubule dynamics as a key mediator of NP-induced damage and a promising therapeutic target.
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Exposure to polystyrene nanoplastics promotes premature cellular senescence through mitochondrial ROS production and dysfunction in pre-differentiated skeletal myoblasts
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This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
Polystyrene microplastics induce skeletal muscle atrophy through disruption of anabolic signaling and mitochondrial function
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Researchers exposed muscle cells to polystyrene microplastics and found dose-dependent muscle atrophy driven by suppressed IGF-1/PI3K/Akt/mTOR anabolic signaling, elevated oxidative stress, and mitochondrial dysfunction—effects comparable to the steroid dexamethasone—suggesting microplastics may be an unrecognized environmental contributor to muscle wasting.
Nanoplastics as disruptors of microtubule dynamics and intracellular trafficking: implications for cellular senescence and ageing
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This review pulls together existing research suggesting that tiny plastic particles lodged in our cells might jam up the internal "delivery system" that moves and clears cellular waste, potentially speeding up aging and cell decline. While plastics have been found in human tissues, scientists still need direct proof that they actually cause this damage in people, so this remains a promising but unconfirmed theory.
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.
Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism
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Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
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