5-hydroxytryptamine 2B Receptor Antagonism with MARY1 Attenuates Maladaptive Repair and Fibrosis Following Ischemic Kidney Injury

Following ischemic kidney injury, unresolved inflammation, epithelial/endothelial-mesenchymal transition, and failed tubule repair drive progression to CKD. We show that MARY1, a selective 5-HT2B receptor antagonist, restores renal function, suppresses inflammation and pro-fibrotic/EMT markers, reduces cell-cycle arrest, and shifts proximal tubule cells toward an adaptive-repair gene signatures in mice. This positions 5-HT2B antagonism as a therapeutic strategy against AKI-to-AKD transition.