Victor G Puelles, James W van der Wolde, Nicola Wanner, Markus W Scheppach, Luise A Cullen-McEwen, Tillmann Bork, Maja T Lindenmeyer, Lukas Gernhold, Milagros N Wong, Fabian Braun, Clemens D Cohen, Michelle M Kett, Christoph Kuppe, Rafael Kramann, Turgay Saritas, Claudia R van Roeyen, Marcus J Moeller, Leon Tribolet, Richard Rebello, Yu By Sun, Jinhua Li, Gerhard Müller-Newen, Michael D Hughson, Wendy E Hoy, Fermin Person, Thorsten Wiech, Sharon D Ricardo, Peter G Kerr, Kate M Denton, Luc Furic, Tobias B Huber, David J Nikolic-Paterson, John F Bertram
The cellular origins of glomerulosclerosis involve activation of parietal epithelial cells (PECs) and progressive podocyte depletion. While mammalian target of rapamycin-mediated (mTOR-mediated) podocyte hypertrophy is recognized as an important signaling pathway in the context of glomerular disease, the role of podocyte hypertrophy as a compensatory mechanism preventing PEC activation and glomerulosclerosis remains poorly understood. In this study, we show that glomerular mTOR and PEC activation-related genes were both upregulated and intercorrelated in biopsies from patients with focal segmental glomerulosclerosis (FSGS) and diabetic nephropathy, suggesting both compensatory and pathological roles...
September 19, 2019: JCI Insight