title: Aberrant mTORC1 activation kills tubular cells by inactivating miR148b-3p.
abstract: A new study by Kuwagata et al. now shows that aberrant activation of the mechanistic target of rapamycin complex 1 in renal tubular cells causes their injury and cell death by enhancing endoplasmic reticulum stress and cell death pathway under diabetic conditions. The study has revealed a novel molecular mechanism in which mechanistic target of rapamycin complex 1 stimulates the tumor necrosis factor signaling by attenuating miR-148b-3p, thereby deteriorating renal tubular cell dysfunction under diabetic conditions.
authors.affiliation: Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA; Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA; Division of Nephrology, Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA. Electronic address: inokik@umich.edu.
authors.forename: Ken
authors.initials: K
authors.lastname: Inoki
mesh_terms: D000818:Animals; D017209:Apoptosis; D000076222:Mechanistic Target of Rapamycin Complex 1; D047889:Receptors, Tumor Necrosis Factor, Type II; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases
chemical_list: D047889:Receptors, Tumor Necrosis Factor, Type II; D000076222:Mechanistic Target of Rapamycin Complex 1; D058570:TOR Serine-Threonine Kinases
keywords: diabetic nephropathy; mTORC1; microRNA