Figure 8.

Pod-p53 regulates the glomerular hyperplastic phenotypes in the progression of AS. Podocyte foot process structures are maintained in early stage of AS. Progressive disruption of foot process structures gradually induces renal dysfunction. Pod-p53 deletion in AS mouse enhances podocyte foot process effacement and induces aberrant filopodia formation. Pod-p53^−/− AS mouse had increased number of proliferative PECs and podocytes. Gene-expression patterns were altered, and secreted type of factors that modify cell proliferation and migration were enhanced in pod-p53^−/− AS mouse. These secreted factors may influence proliferation of PECs and crescent formation in AS progression. Furthermore, p53 expression is suppressed in the glomeruli of AS mouse at late stage and this contributes to the hyperplastic glomerular disorder and progression of renal dysfunction in AS.