Podocyte injury is the hallmark of proteinuric kidney diseases， such as FSGS and minimal change disease， and destabilization of the podocyte's actin cytoskeleton contributes to podocyte dysfunction in many of these conditions. Although agents， such as glucocorticoids and cyclosporin， stabilize the actin cytoskeleton， systemic toxicity hinders chronic use. We previously showed that loss of the kidney-enriched zinc finger transcription factor Krüppel-like factor 15 (KLF15) increases susceptibility to proteinuric kidney disease and attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte.
Podocyte injury is the hallmark of proteinuric kidney diseases， such as FSGS and minimal change disease， and destabilization of the podocyte's actin cytoskeleton contributes to podocyte dysfunction in many of these conditions. Although agents， such as glucocorticoids and cyclosporin， stabilize the actin cytoskeleton， systemic toxicity hinders chronic use. We previously showed that loss of the kidney-enriched zinc finger transcription factor Krüppel-like factor 15 (KLF15) increases susceptibility to proteinuric kidney disease and attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte.
