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In the subsequent years, several observational studies have yielded conflicting results.4043 Notably, most of the available information is drawn from the subgroup of exendin-4-based drugs, which differ structurally from human GLP-1

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On the other hand, suppressing ferroptosis might enhance an M2 phenotype that is anti-inflammatory, which may help decrease tissue damage and inflammation ( Depletion of glutathione peroxidase 4 (GPX4), an enzyme that lowers lipid hydroperoxides and inhibits lipid peroxidation, is the main cause of ferroptosis in macrophages ( By increasing inflammation and blocking tissue healing, ferroptosis in macrophages in ARDS increases the severity of lung damage