Carvedilol Confers Ferroptosis Resistance in HL-1 Cells by Upregulating GPX4, FTH1, and FTL1 and Inducing Metabolic Remodeling Under Hypoxia/Reoxygenation DOI Creative Commons

Yi-Chin Li,

Mei‐Ling Cheng

Antioxidants, Год журнала: 2024, Номер 14(1), С. 7 - 7

Опубликована: Дек. 24, 2024

Hypoxia/reoxygenation (HR) often occurs under cardiac pathological conditions, and HR-induced oxidative stress usually leads to cardiomyocyte damage. Carvedilol, a non-selective β-blocker, is used clinically treat ischemia diseases. Moreover, Carvedilol has also been reported have an antioxidant ability by reducing lipid peroxidation. However, the mechanism of inhibit peroxidation still elusive. To explore protective resist on cardiomyocytes, HL-1 cells were cultured normoxia, hypoxia, HR treated with investigate alteration metabolism, protein expression, mRNA level explain its mechanism. The study found that upregulated glutathione peroxidase 4 (GPX4) expression metabolic remodeling HR. Also, promoted ferroptosis-related genes, ferritin heavy chain 1 (FTH1) light (FTL1) levels, reduce both hypoxia In conclusion, our explores which inhibits ferroptosis upregulating GPX4, FTH1, FTL1 levels downregulate provides potential strategy for using in clinical applications, inspiring further research development area heart

Язык: Английский

Carvedilol Confers Ferroptosis Resistance in HL-1 Cells by Upregulating GPX4, FTH1, and FTL1 and Inducing Metabolic Remodeling Under Hypoxia/Reoxygenation DOI Creative Commons

Yi-Chin Li,

Mei‐Ling Cheng

Antioxidants, Год журнала: 2024, Номер 14(1), С. 7 - 7

Опубликована: Дек. 24, 2024

Hypoxia/reoxygenation (HR) often occurs under cardiac pathological conditions, and HR-induced oxidative stress usually leads to cardiomyocyte damage. Carvedilol, a non-selective β-blocker, is used clinically treat ischemia diseases. Moreover, Carvedilol has also been reported have an antioxidant ability by reducing lipid peroxidation. However, the mechanism of inhibit peroxidation still elusive. To explore protective resist on cardiomyocytes, HL-1 cells were cultured normoxia, hypoxia, HR treated with investigate alteration metabolism, protein expression, mRNA level explain its mechanism. The study found that upregulated glutathione peroxidase 4 (GPX4) expression metabolic remodeling HR. Also, promoted ferroptosis-related genes, ferritin heavy chain 1 (FTH1) light (FTL1) levels, reduce both hypoxia In conclusion, our explores which inhibits ferroptosis upregulating GPX4, FTH1, FTL1 levels downregulate provides potential strategy for using in clinical applications, inspiring further research development area heart

Язык: Английский

Процитировано

0