title: MTOR regulates autophagic flux in the glomerulus.
abstract: Sirolimus (rapamycin), an inhibitor of the mechanistic target of rapamycin (MTOR), was originally proposed as an immunosuppressant to prevent rejection of solid organ transplants. There were expectations that MTOR inhibitors would replace nephrotoxic calcineurin inhibitors (CNIs). Despite its potential advantages, evidence that sirolimus causes de novo or worsening proteinuria is unequivocal. Given the well-recognized proteinuric effect of MTOR inhibitors, we were interested in understanding its role in maintaining the glomerular filtration barrier. To investigate this in vivo, we developed a mouse model with a podocyte selective deletion of the Mtor gene (Mtor pod-KO).
authors.affiliation: Samuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario Canada.
authors.forename: Davide P
authors.initials: DP
authors.lastname: Cinà
authors.forename: Tuncer
authors.initials: T
authors.lastname: Onay
authors.forename: Aarti
authors.initials: A
authors.lastname: Paltoo
authors.forename: Chengjin
authors.initials: C
authors.lastname: Li
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Maezawa
authors.forename: Javier
authors.initials: J
authors.lastname: De Arteaga
authors.forename: Andrea
authors.initials: A
authors.lastname: Jurisicova
authors.forename: Susan E
authors.initials: SE
authors.lastname: Quaggin
mesh_terms: D000818:Animals; D001343:Autophagy; D006801:Humans; D007678:Kidney Glomerulus / Q000201:enzymology* / Q000473:pathology*; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D050199:Podocytes / Q000378:metabolism / Q000473:pathology; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*
chemical_list: D058570:TOR Serine-Threonine Kinases