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Regulating Autophagy as a Therapeutic Target for Diabetic Nephropathy

  • Munehiro KitadaEmail author
  • Yoshio Ogura
  • Itaru Monno
  • Daisuke Koya
Microvascular Complications—Nephropathy (M Afkarian, Section Editor)
Part of the following topical collections:
  1. Topical Collection on Microvascular Complications—Nephropathy

Abstract

Purpose of Review

Autophagy promotes cellular health in response to various cellular stresses and to changes in nutrient conditions. In this review, we focus on the role of autophagy in the pathogenesis of diabetic nephropathy and discuss the regulation of autophagy as a new therapeutic target for the suppression of diabetic nephropathy.

Recent Findings

Previous studies have indicated that autophagy deficiency or insufficiency in renal cells, including podocytes, mesangial cells, endothelial cells and tubular cells, contributes to the pathogenesis of diabetic nephropathy. Alterations in the nutrient-sensing pathways, including mammalian target of rapamycin complex1 (mTORC1), AMP-activated kinase (AMPK) and Sirt1, due to excess nutrition in diabetes are implicated in the impairment of autophagy.

Summary

Maintaining both basal and adaptive autophagy against cellular stress may protect the kidney from diabetes-induced cellular stresses. Therefore, the activation of autophagy through the modulation of nutrient-sensing pathways may be a new therapeutic option for the suppression of diabetic nephropathy.

Keywords

Diabetic nephropathy Autophagy mTORC1 Sirt1 

Notes

Compliance with Ethical Standards

Conflict of Interest

Boehringer Ingelheim, Mitsubishi Tanabe Pharma, Kyowa Hakko Kirin, Taisho Toyama Pharmaceutical Co., and Ono Pharmaceutical Co. contributed to establishing the Division of Anticipatory Molecular Food Science and Technology. Munehiro Kitada, Yoshio Ogura, Itaru Monno, and Daisuke Koya declare that there are no conflicts of interest associated with this manuscript.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Funding

This work was financially supported by a Grant for Promoted Research from Kanazawa Medical University (S2016-11) to M.K.; a Grant-in-Aid for Challenging Exploratory Research (16 K15472), the Science Research Promotion Fund for the promotion and mutual corporation for private schools of Japan, and a Grant for Collaborative Research from Kanazawa Medical University (C2015-2) to D.K.

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Copyright information

© Springer Science+Business Media New York 2017

Authors and Affiliations

  • Munehiro Kitada
    • 1
    • 2
    Email author
  • Yoshio Ogura
    • 1
  • Itaru Monno
    • 1
  • Daisuke Koya
    • 1
    • 2
  1. 1.Department of Diabetology and EndocrinologyKanazawa Medical UniversityUchinadaJapan
  2. 2.Division of Anticipatory Molecular Food Science and Technology, Medical Research InstituteKanazawa Medical UniversityUchinadaJapan

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