KRT20 suppresses the exosomal secretion of PRDX2 to mitigate ferroptosis in acute kidney injury

Acute kidney injury (AKI) is a commonly observed but poorly understood clinical syndrome. Keratin 20 (KRT20), a key component of intermediate filaments, is generally known as a biomarker of renal tubular injury, but its role in kidney disease remains unclear. We have verified KRT20 induction in renal proximal tubules in experimental models of AKI and also in human patient samples. We further suggest the involvement of Fosb in KRT20 induction. Upon induction, KRT20 may interact with and sequester PRDX2 in renal tubular cells to prevent ferroptosis, thus providing a novel therapeutic target for AKI.