Improved understanding of signal transduction processes in podocytes not only has increased our knowledge of the mechanisms of diseases but also identified new potential therapeutic strategies to reverse foot process effacement, limit apoptosis, and control podocyte differentiation state (see below).
A tamoxifen-inducible model of PAX2 reexpression reveals morphologic changes similar to those of human CG, with podocyte proliferation, and points toward a direct regulatory effect of both WT1 and nephrin expression as a cause of foot process effacement and proteinuria.
Inactivation of MafB results in downregulation of NPHS1, NPHS2, and CD2AP, genes that encode for critical proteins of the SD, and consequent foot process effacement.
As demonstrated by more than one animal model where nephrin or podocin is missing, defects of SD composition do not interfere with foot process formation and interdigitation, suggesting that SD formation is a phenomenon secondary to foot process formation, but the maintenance of foot process structure is dependent on SD proteins (reviewed in Kriz (27)).
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