Perspectives on blockade of TGFβ overexpression

Abstract

Many approaches to blocking profibrotic TGFβ overexpression are under way. Therapeutic targeting of TGFβ–Smad signaling holds promise for slowing or halting progressive renal disease. In this issue, Fukasawa et al., using the unilateral ureteral obstruction model, provide a new target for therapeutic intervention by identifying loss of the Smad corepressors Ski and SnoN as a mechanism that amplifies the profibrotic actions of TGFβ