Work

Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes

Year: 2025

Type: article

Abstract: Microplastics (MPs) are ubiquitous in the global biosphere, have widespread contact with humans, and increase exposure risks. Increasing evidence indicates that MPs exposure increases the risks of cardiovascular disease, however, a comprehensive exploration of the fundamental cellular mechanisms has yet to be undertaken. In this study, we used AC16 cells as a model and exposed them to 10 to 50 μg/mL of polystyrene MPs (PS-MPs), chosen based on the average daily intake and absorption of MPs by humans, to investigate their roles and mechanisms in cell injury. Proteomic analysis reveals that PS-MP-induced differentially expressed genes were enriched on endoplasmic reticulum (ER) stress and autophagy-related entries. The findings from immunofluorescence and western blotting provided further verification of the activation of ER stress by PS-MPs. Although the expression of LC3-II, a canonical autophagy marker was increased, PS-MPs inhibited autophagic flux instead of inducing autophagy. Importantly, ER stress not only contributes to PS-MPs-induced cell injury but also involved in PS-MPs-induced autophagic flux inhibition. Furthermore, the inhibition of autophagy, and the partial restoration of cell injury induced by PS-MPs was achieved through the activation of autophagy. Overall, the results reveal that activation of ER stress and inhibition of autophagic flux plays a significant role in the cell injury caused by PS-MPs in human cardiomyocytes, offering a novel perspective on the mechanism behind MPs-induced cardiomyocyte toxicity.

Source: The Science of The Total Environment

DOI: 10.1016/j.scitotenv.2025.179048