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No formal recovery period is required and most patients resume normal activities immediately

Hypoxia activates Kupffer cells and hepatic stellate cells to release proinflammatory cytokines, which recruit additional inflammatory cells 3,5

The therapeutic manipulation of ferroptosis has gained interest in diseases where iron and oxidative stress contribute to pathological mechanisms [93, 94]

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The NLRP3 inflammasome then facilitates the dimerization and activation of caspase-1, leading to the cleavage of pro-IL-1, pro-IL-18, and GSDMD into their active forms