Feed

As air pollution intensifies, the health risks associated with PM2.5 have gained increasing global attention. Previous research has established a link between PM2.5 exposure and increased risk of cardiovascular diseases (CVDs), yet the underlying mechanisms remain unclear. In this study, we demonstrate that PM2.5 induces ferroptosis in myocardial cells both in vitro and in vivo. We also show that PM2.5 exposure increases lipid peroxidation levels and cellular iron content while depleting glutathione (GSH). Notable alterations in the expression of transferrin receptor protein 1 (TfR1), ferritin light chain (FTL), and ferritin heavy chain (FTH) suggest that the dysfunction in iron uptake and storage plays a pivotal role in ferroptosis. Moreover, we observed that PM2.5 exposure upregulates p53 expression, which transcriptionally regulates TfR1 synthesis. This leads to increased iron influx into cells, causing iron overload and ultimately contributing to ferroptosis and myocardial injury. In conclusion, our findings suggest that PM2.5 promotes ferroptosis in the myocardium via the p53/TfR1 pathway.