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Polystyrene microplastics-induced ROS overproduction disrupts the skeletal muscle regeneration by converting myoblasts into adipocytes
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Researchers found that polystyrene microplastics impaired skeletal muscle repair in mice by triggering excess production of reactive oxygen species (ROS) inside muscle stem cells. This oxidative stress redirected muscle stem cells to become fat cells instead of new muscle fibers, resulting in increased fat deposits and reduced muscle fiber size. The study suggests that microplastic exposure could interfere with the body's natural ability to regenerate and maintain muscle tissue.
The environmental problem of Microplastics (MPs) pollution poses a great threat to human and animal health, which has attracted global attention. The physiological integrity of skeletal muscle is extremely important for the survival of animals. Here, we investigated the effect of two size polystyrene microplastics (PS-MPs, 1-10 µm and 50-100 µm) on the growth of anterior tibial (TA) muscle and repair after injury in mice. Results showed that the regeneration of skeletal muscle was delayed by PS-MPs exposure and was negatively correlated with particle size. H&E staining and Oil red O staining showed that PS-MPs exposure reduced the average cross-sectional area (CSA) and diameter of the muscle fibers, increased lipid deposition. Further mechanistic research displayed that though PS-MPs treatment did not affect cell viability of myoblast, it aggravated intracellular ROS generation and oxidative stress, inhibited myogenic differentiation by decreasing the phosphorylation of p38 MAPK, and promote adipogenic differentiation by increasing the expression of NF-κB, which could be alleviated by NAC. In brief, our data demonstrated that the ROS overproduction caused by PS-MPs disturbed the regeneration of skeletal muscle and directed the fate of satellite cells in mice.
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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.
Microplastics induce insulin resistance by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro
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Researchers exposed human muscle cells to polystyrene micro and nanoplastics and found that the particles caused insulin resistance, meaning the cells could not properly absorb sugar from the blood. The plastics damaged the cells' mitochondria (the energy-producing structures) and triggered harmful oxidative stress, but a mitochondria-protecting antioxidant reversed the damage. This study suggests that microplastic exposure could contribute to metabolic problems like type 2 diabetes by impairing how muscles process sugar.
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.
Polystyrene microplastics (PS-MPs) disturb skeleto-muscular energy metabolism and tissue architecture following sub-acute exposure: A dose-responsive study
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Wistar rats given polystyrene microplastics in drinking water (0.5–50 mg/L) for 28 days showed dose-dependent disruption of skeletal muscle energy metabolism — including reduced ATP production and altered mitochondrial activity — along with histological changes in muscle tissue architecture.
Exposome on skeletal muscle system: a mini-review
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This mini-review examines how environmental exposures, including microplastics, heavy metals, and other pollutants, affect skeletal muscle biology. Evidence indicates that microplastics may delay muscle regeneration and promote fat cell formation through specific signaling pathways, suggesting that cumulative environmental exposures could have meaningful effects on muscle health across the lifespan.
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