Protein phosphatases and podocyte function

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Purpose of review

Deregulation of protecting factor signaling actions in podocytes has emerged as an alternative pathway of podocyte injury mechanisms. Here, we review recent knowledge that highlighted how podocyte protecting factors are modulated by protein phosphatases.

Recent findings

Protein tyrosine kinases and phosphatases participate in many, if not all, aspects of cellular function by turning on or off multiple signaling cascades and podocytes are no exception. Modulation of tyrosine residue phosphorylation of podocyte factors such as nephrin, vascular endothelial growth factor, insulin receptors and substrates has been shown to promote podocyte damage and cell death that contributed to multiple glomerular diseases. Protein phosphatase activity can cause either an increase [Src homology 2 domain-containing phosphatase 2 (SHP-2)] or a decrease [Protein tyrosine phosphatase1B (PTP1B), SHP-1 and SH2 domain–containing 5′-inositol phosphatase 2 (SHIP2)] in nephrin tyrosine phosphorylation depending on which podocyte injury model was used. Insulin resistance is closely linked to the development and progression of renal disease. Expression of PTP1B, SHP-1, phosphatase and tensin homolog and SHIP2 are potential mechanisms of podocytes insulin resistance in diabetic kidney disease.


Tight regulation of protein phosphatases is critical to maintain cell homeostasis and may offer new perceptive targets to restore protecting factor actions in order to prevent podocyte dysfunction and glomerular diseases.

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