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Mechanistically, by activating Nrf2, the combined effects may offset the potential risk of iron overload associated with HO-1 induction, consistent with the findings reported by Luo et al

fermentum was localized for several hours after oral administration (Supplementary Fig

Therefore, understanding the cellular and molecular mechanisms that contribute to chronic radiodermatitis onset and progression is essential for developing targeted therapies that can prevent or reduce the severity of fibrotic changes, ultimately aiming to preserve patient quality of life and improve cancer care post-radiotherapy