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. Author manuscript; available in PMC: 2019 Jun 6.
Published in final edited form as: Nat Rev Nephrol. 2016 Aug 1;12(10):587–609. doi: 10.1038/nrneph.2016.108

Figure 2. Roles of mTOR complexes in the kidney as revealed using pharmacological inhibition or cell-specific genetic deletion of mTOR1 or mTOR2.

Figure 2

mTOR complexes are expressed throughout the nephron and regulate homeostasis of all resident parenchymal and non-parenchymal cells. Disruption of mTOR signalling results in various pathologies that are dependent on cellular location and whether TORC1 or TORC2 is targeted: proximal TEC downregulate megalin resulting in proteinuria, while distal TEC exposure leads to polyuria and natriuresis, and inflammatory cell infiltrate and fibroblastic responses are reduced following IRI. Within the glomerulus, podocyte function is disrupted leading to frank proteinuria and glomerulosclerosis, while endothelial cell proliferation is limited. Abbreviations: ERK, extracellular signal-regulated kinase; NKCC, Na-K-Cl co-transporter; MR, mineralocorticoid receptor; SGK1, serum and glucocorticoid inducible kinase 1; ENaC, Epithelial sodium channel; IRI, ischemia-reperfusion injury; mTORi, mTOR inhibition.