Podocyte depletion leads to glomerulosclerosis, but whether an impaired capacity of
podocytes to respond to hypertrophic stress also causes glomerulosclerosis is unknown. We
generated transgenic Fischer 344 rats that express a dominant negative AA-4E-BP1
transgene driven by the podocin promoter; a member of the mammalian target of rapamycin
complex 1 (mTORC1) pathway, 4E-BP1 modulates cap-dependent translation, which is a
key determinant of a cell's hypertrophic response to nutrients and growth factors. AA-4E-BP1 …