TGFβ1-dependent podocyte dysfunction.

PURPOSE OF REVIEW

The glomerular filtration barrier is a unique structure characterized by a specialized framework of podocytes. Transforming growth factor-β1 (TGFβ1) upregulation occurs in virtually all chronic kidney diseases and is associated with podocyte injury and proteinuria. This review is aimed at describing the latest advances made in the understanding of TGFβ-induced podocyte injury.

RECENT FINDINGS

During the past decade, progress has been made in understanding the biology and mechanisms of TGFβ-induced podocyte injury. Most forms of glomerular diseases, including diabetic nephropathy, are associated with increased TGFβ1 signaling and thus TGFβ1 plays a central role in the pathogenesis of podocytopathy. The mechanism of podocyte injury is complex, involving a number of independent and overlapping cellular and molecular pathways. This review will examine these direct and indirect effects of TGFβ1 on podocyte dysregulation as reflected in their growth, differentiation, and motility.

SUMMARY

These new developments in understanding the podocyte response to injury are critical for establishing better therapeutic interventions that target specific pathways, which otherwise could lead to irreversible injury.