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Proximal Tubule mTORC1 Is a Central Player in the Pathophysiology of Diabetic Nephropathy and Its Correction by SGLT2 Inhibitors

Authors
  • Kogot-Levin, Aviram1
  • Hinden, Liad2
  • Riahi, Yael1
  • Israeli, Tal1
  • Tirosh, Boaz3
  • Cerasi, Erol1
  • Mizrachi, Ernesto Bernal4
  • Tam, Joseph2
  • Mosenzon, Ofri1
  • Leibowitz, Gil1
  • 1 Diabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
  • 2 Obesity and Metabolism Laboratory, Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel
  • 3 Stress Signaling Laboratory, School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem, Israel
  • 4 Department of Internal Medicine, Division of Endocrinology, Metabolism and Diabetes, Miller School of Medicine, University of Miami, Miami, FL, USA
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Jul 28, 2020
Volume
32
Issue
4
Identifiers
DOI: 10.1016/j.celrep.2020.107954
PMID: 32726619
PMCID: PMC7397516
Source
PubMed Central
Keywords
License
Unknown

Abstract

Kogot-Levin et al. show that treatment with sodium-glucose cotransporter 2 inhibitors (SGLT2i) attenuates the progression of diabetic kidney disease (DKD), which is the leading cause of end-stage renal disease. The nutrient sensor mTORC1 is a critical node that mediates kidney dysfunction in diabetes and the protective effects of SGLT2i by regulating fibrogenesis.

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