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Through the upregulation of survival pathways and the downregulation of cell death signals, it may create conditions that support cellular persistence and function

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Moreover, microbial metabolites such as short-chain fatty acids and secondary bile acids influence thyroid hormone metabolism by regulating hepatic deiodinase activity, enterohepatic circulation, and tissue sensitivity to T 3 (Miquel et al., 2013

Emerging research suggests that a decline in glutathione levels might precede GPX4 inactivation, further weakening the antioxidative defenses, escalating lipid ROS accumulation, and driving ferroptosis [16]