{Reference Type}: Journal Article
{Title}: SiO 2 Induces Iron Overload and Ferroptosis in Cardiomyocytes in a Silicosis Mouse Model.
{Author}: Wang YH;Li N;Guan Y;Li T;Zhang Y;Cao H;Yu ZH;Li ZH;Li SY;Hu JH;Zhou WX;Qin SS;Li S;Yao SQ;
{Journal}: Biomed Environ Sci
{Volume}: 37
{Issue}: 6
{Year}: 2024 Jun 20
{Factor}: 2.831
{DOI}: 10.3967/bes2024.087
{Abstract}: <B>UNASSIGNED: </B>The aim of this study was to explore the role and mechanism of ferroptosis in SiO 2-induced cardiac injury using a mouse model.<BR><B>UNASSIGNED: </B>Male C57BL/6 mice were intratracheally instilled with SiO 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.<BR><B>UNASSIGNED: </B>SiO 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 SiO 2-induced mitochondrial damage and myocardial injury. SiO 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.<BR><B>UNASSIGNED: </B>Iron overload-induced ferroptosis contributes to SiO 2-induced cardiac injury. Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO 2 cardiotoxicity, potentially via modulation of the Nrf2 pathway.