This reduction in Smurf2 subsequently prevented the Smurf2-mediated ubiquitination of ChREBP, leading to ChREBP accumulation and the up regulation of tubular injury and fibrosis markers.<h4>Conclusion</h4>These findings indicate that RetSat promotes TIF in DKD by disrupting the Smurf2-ChREBP ubiquitination axis, highlighting RetSat as a promising therapeutic target for DKD. Here, RETSAT is linked to diabetic kidney disease.