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

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

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.