%0 Journal Article
%T SiO 2 Induces Iron Overload and Ferroptosis in Cardiomyocytes in a Silicosis Mouse Model.
%A Wang YH
%A Li N
%A Guan Y
%A Li T
%A Zhang Y
%A Cao H
%A Yu ZH
%A Li ZH
%A Li SY
%A Hu JH
%A Zhou WX
%A Qin SS
%A Li S
%A Yao SQ
%J Biomed Environ Sci
%V 37
%N 6
%D 2024 Jun 20
%M 38988112
%F 2.831
%R 10.3967/bes2024.087
%X <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.