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recently showed that direct GPx4 overexpression in the cellular models (A549, H460 and H1299 and H23) of non-small cell lung carcinoma (NSCLC) prevented the radiation-induced lipid peroxidation and, in turn, contributed to radioresistance by blocking the ferroptosis mode of cell death [56]

Each agent differs in molecular structure, half-life, and dosing frequency, but all share the core mechanism of GLP-1 receptor activation that influences multiple organ systems, including indirect effects on hepatic function

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Now, we find ourselves in yet another shift