In acute kidney injury (AKI), dysregulated tissue regeneration can promote fibrosis and chronic kidney disease. Sustained SOX9 expression after AKI is a key promoter of fibrosis, according to a new study by Sanjeev Kumar and colleagues.

Epigenetic analyses suggest that cells with persistent SOX9 expression have a progenitor cell-like phenotype with patterns of chromatin reorganization that are associated with nephrogenesis and are distinct from those of SOX9– cells.