SiO 2 Induces Iron Overload and Ferroptosis in Cardiomyocytes in a Silicosis Mouse Model.
Biomed Environ Sci
; 37(6): 617-627, 2024 Jun 20.
Article
em En
| MEDLINE
| ID: mdl-38988112
ABSTRACT
Objective:
The aim of this study was to explore the role and mechanism of ferroptosis in SiO 2-induced cardiac injury using a mouse model.Methods:
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.Results:
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.Conclusion:
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.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Silicose
/
Dióxido de Silício
/
Sobrecarga de Ferro
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Miócitos Cardíacos
/
Modelos Animais de Doenças
/
Ferroptose
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Camundongos Endogâmicos C57BL
Limite:
Animals
Idioma:
En
Revista:
Biomed Environ Sci
Assunto da revista:
SAUDE AMBIENTAL
Ano de publicação:
2024
Tipo de documento:
Article
País de afiliação:
China