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Emerging role of autophagy in kidney function, diseases and aging

  • Tobias B. Huber(corresponding author)
    ,
  • Charles L. Edelstein
    ,
  • Björn Hartleben
    ,
  • Ken Inoki
    ,
  • Man Jiang
    ,
  • Daisuke Koya
*Corresponding author for this work
  • University of Freiburg
    ,
  • University of Colorado Anschutz Medical Campus
    ,
  • University of Michigan, Ann Arbor
    ,
  • Cellular Biology and Anatomy
    ,
  • Kanazawa Medical University
    ,
  • Shiga University of Medical Science
Scholary Output:
Contribution to journal
Review article
 Peer-review

Open access

Abstract

Autophagy is a highly conserved process that degrades cellular long-lived proteins and organelles. Accumulating evidence indicates that autophagy plays a critical role in kidney maintenance, diseases and aging. Ischemic, toxic, immunological, and oxidative insults can cause an induction of autophagy in renal epithelial cells modifying the course of various kidney diseases. This review summarizes recent insights on the role of autophagy in kidney physiology and diseases alluding to possible novel intervention strategies for treating specific kidney disorders by modifying autophagy.

Publication Information

Output type

Scholary Output:
Contribution to journal
Review article
 Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 1009-1031 (23 pages)

Journal (Volume, Issue Number)

Autophagy (Volume 8, Issue 7)

Publication milestones

  • Published - 07/2012

Publication status

Published - 07/2012

ISSN

1554-8627

Publication IDs

  • Scopus: 84866142024
  • PubMed: 22692002

Access to documents

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Scopus
citations
253, opens in new tab
SciVal
citations
185
SciVal
FWCI
1.70
SciVal
Author count
14
SciVal
Paper percentile
99
SciVal
Top percentile
1
Fractional count
2
Fractional count
0.14
Fractional count
12
Fractional count
0.86
Fractional count
2
Fractional count
1

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Citation count
233
Captures
136
Social media
11

Funding Details

We thank members of our laboratories for critical reading of the manuscript. This work was supported in part by Deutsche Forschungsgemeinschaft grant KFO 201 (to T.B.H.), by the Excellence Initiative of the German Federal and State Governments EXC 294 (to T.B.H.), by GerontosysII—NephAge (031589GA) (to T.B.H.), by the U.S.National Institutes of Health (RO1DK056851 and DK074835 to C.E., DK058831 and DK087843 to Z.D., DK083491 to K.I.), by the U.S. Veterans Administration (to Z.D. and to W.L.), by Grant-in-Aid For Diabetic Nephropathy Research from the Ministry of Health, Labour and Welfare of Japan (to D.K.), and the KAKENHI 21591148 (to D.K.) and 00452235 (to S.K.).
FundersFunding numbers
GerontosysII
031589GA
U.S. Department of Veterans Administration BLR&D
-
U.S.National Institutes of Health
DK083491, DK087843, RO1DK056851, DK058831, DK074835
NIDDK
R01DK083491
DFG
KFO 201
MHLW
21591148, 00452235