Targeting PKM2-dependent glycolysis reprogrammes monocytes into Cadm1⁺ macrophages to promote mucosal repair and attenuate colitis progression

The authors aimed to determine whether modulating macrophage metabolism, specifically targeting PKM2-dependent glycolysis, could promote mucosal healing in ulcerative colitis (UC) without increasing the risk of tumorigenesis. Their findings indicate that PKM2 depletion in macrophages enhances intestinal barrier function and promotes the differentiation of reparative Cadm1⁺ macrophages, ultimately leading to improved mucosal repair and reduced colitis progression in mouse models. Importantly, this approach was associated with a decrease in tumorigenesis, suggesting a potential therapeutic strategy for UC.