4.7 Review

Autophagy in kidney disease and aging: lessons from rodent models

Journal

KIDNEY INTERNATIONAL
Volume 90, Issue 5, Pages 950-964

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.kint.2016.04.014

Keywords

acute kidney injury; aging; autophagy; endothelium; glomerulus; kidney; kidney transplantation; mTOR; podocyte; polycystic kidney disease

Funding

  1. INSERM
  2. l'Agence Nationale de la Recherche (ANR) of France
  3. Lefoulon-Delalande Foundation
  4. Francophone Diabetes Society
  5. German Research Foundation (DFG) [CRC 1140, CRC 992]
  6. Heisenberg program
  7. European Research Council-ERC grant [616891, 311255]
  8. BMBF-Joint transnational grant [01KU1215]
  9. STOP-FSGS [01GM1518C]
  10. Else-Kroner Fresenius Stiftung-NAKSYS
  11. Excellence Initiative of the German Federal and State Governments [GSC-4, EXC294]
  12. Excellence Initiative of the German Federal and State Governments (Spemann Graduate School)
  13. [HU 1016/8-1]
  14. European Research Council (ERC) [311255, 616891] Funding Source: European Research Council (ERC)

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Autophagy is a highly regulated lysosomal protein degradation pathway that removes protein aggregates and damaged or excess organelles to maintain intracellular homeostasis and cell integrity. Dysregulation of autophagy is involved in the pathogenesis of a variety of metabolic and age-related diseases. Growing evidence suggests that autophagy is implicated in cell injury during renal diseases, both in the tubulointerstitial compartment and in glomeruli. Nevertheless, the impact of autophagy on renal disease progression and aging is still not fully understood. This review summarizes the recent advances in understanding the role of autophagy for kidney disease and aging.

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