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Polystyrene microplastics-induced ROS overproduction disrupts the skeletal muscle regeneration by converting myoblasts into adipocytes

Journal of Hazardous Materials 2021 193 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Shengchen Wang, Shengchen Wang, Shengchen Wang, Yue Wang, Liu Jing, Liu Jing, Shengchen Wang, Yujie Yao, Shengchen Wang, Yujie Yao, Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shengchen Wang, Yue Wang, Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Yujie Yao, Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu

Summary

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.

Polymers
Body Systems

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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