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In the present study, we have evaluated whether an antioxidant agent, glutathione, prevents the development of NASH from FL
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HO1, a target of Nrf2, is a cytoprotective enzyme that degrades hemoglobin into CO, iron, and biliverdin 37 , and its function in ferroptosis is contradictory, suggesting that dual, protective, or detrimental effects depend on the degree of cellular iron levels and ROS, indicating enhanced ferroptosis via the Nrf2/HO1 axis in our study 23,38
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