Excessive ultra-processed foods exposure aggravates ulcerative colitis via macrophage ferroptosis

This is the authors' abstract. We don't add key points for this paper.

, and reactive oxygen species (ROS) with statistical significance (p < 0.05). Crucially, ALKBH5 overexpression restored GCLM-mediated antioxidant defenses and mitigated ferroptosis in RAW264.7 cells (p < 0.05). Immunofluorescence confirmed KS-mediated suppression of the ALKBH5-GCLM axis in clinical specimens, exhibiting strong correlation with UC (p < 0.05). Our findings establish UPFs-derived KS as a novel environmental driver of UC pathogenesis through regulation of macrophage ferroptosis. These results identify the KS-ALKBH5-GCLM-ferroptosis axis as a promising therapeutic target for UC intervention.