Sanqiao Yao

In the published article, there were errors in Figure 3B-C, Figure 4E-F, and Figure 7A-B as published. During the transwell assay and scratch test procedures, we used the equipment's default image naming system for batch exports, which led to difficulties in distinguishing between intervention groups during image selection and resulted in incorrect image placement. Given that a significant amount of time has elapsed since the publication, the original data associated with these results are no longer available, we therefore carried out independent repeat experiments and achieved consistent outcomes with the initial findings. As a result, the relevant images and their quantitative data in Figure 3B-E The corrected Figure 7 and its caption appear below.

Objective The aim of this study was to explore the role and mechanism of ferroptosis in SiO2-induced 2-induced cardiac injury using a mouse model. Methods Male C57BL/6 mice were intratracheally instilled with SiO2 2 to create a silicosis model. Ferrostatin-1 (Fer-1) and deferoxamine (DFO) were used to suppress ferroptosis. Serum biomarkers, oxidative stress markers, histopathology, iron content, and the expression of ferroptosis-related proteins were assessed. Results SiO2 2 altered serum cardiac injury biomarkers, oxidative stress, iron accumulation, and ferroptosis markers in myocardial tissue. Fer-1 and DFO reduced lipid peroxidation and iron overload, and alleviated SiO2-induced 2-induced mitochondrial damage and myocardial injury. SiO2 2 inhibited Nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant genes, while Fer-1 more potently reactivated Nrf2 compared to DFO. Conclusion Iron overload-induced ferroptosis contributes to SiO2-induced 2-induced cardiac injury. Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO2 2 cardiotoxicity, potentially via modulation of the Nrf2 pathway.