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Spatiotemporal analysis of Crohn's disease reveals PECAM2 signaling at the basis of inflammation-to-fibrosis transition (JCC 2025)
Crohn’s disease (CD) can lead to intestinal fibrosis, a serious complication with no effective drug treatments. In a recent study, the authors discovered CD-associated fibrosis driven by PECAM1-CD38 interaction. In parallel, ApoA signaling emerged as relevant for maintaining epithelial and stromal homeostasis. CD38 signaling inhibition effectively reduced colitis symptoms in the TNBS-induced model of chronic inflammation, pointing to new therapeutic possibilities.