PMID- 37442108
OWN - NLM
STAT- MEDLINE
DCOM- 20231004
LR  - 20231024
IS  - 2235-3186 (Electronic)
IS  - 1660-8151 (Linking)
VI  - 147
IP  - 10
DP  - 2023
TI  - The Interplay of Autophagy and Oxidative Stress in the Kidney: What Do We Know?
PG  - 627-642
LID - 10.1159/000531290 [doi]
AB  - BACKGROUND: Autophagy, as an indispensable metabolism, plays pivotal roles in 
      maintaining intracellular homeostasis. Nutritional stress, amino acid deficiency, 
      oxidative stress, and hypoxia can trigger its initiation. Oxidative stress in the 
      kidney activates essential signal molecules, like mammalian target of rapamycin 
      (mTOR), adenosine monophosphate-activated protein kinase (AMPK), and silent 
      mating-type information regulation 2 homolog-1 (SIRT1), to stimulate autophagy, 
      ultimately leading to degradation of intracellular oxidative substances and 
      damaged organelles. Growing evidence suggests that autophagy protects the kidney 
      from oxidative stress during acute ischemic kidney injury, chronic kidney 
      disease, and even aging. SUMMARY: This review emphasizes the cross talk between 
      reactive oxygen species (ROS) signaling pathways and autophagy during renal 
      homeostasis and chronic kidney disease according to the current latest research 
      and provides therapeutic targets during kidney disorders by adjusting autophagy 
      and suppressing oxidative stress. KEY MESSAGES: ROS arise through an imbalance of 
      oxidation and antioxidant defense mechanisms, leading to impaired cellular and 
      organ function. Targeting the overproduction of ROS and reactive nitrogen 
      species, reducing the antioxidant enzyme activity and the recovery of the 
      prooxidative-antioxidative balance provide novel therapeutic regimens to 
      contribute to recovery in acute and chronic renal failure. Although, in recent 
      years, great progress has been made in understanding the molecular mechanisms of 
      oxidative stress and autophagy in acute and chronic renal failure, the focus on 
      clinical therapies is still in its infancy. The growing number of studies on the 
      interactive mechanisms of oxidative stress-mediated autophagy will be of great 
      importance for the future treatment and prevention of kidney diseases.
CI  - (c) 2023 S. Karger AG, Basel.
FAU - Guo, Haihua
AU  - Guo H
AD  - Renal Division, Department of Medicine, Medical Center, University of Freiburg, 
      Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
FAU - Bechtel-Walz, Wibke
AU  - Bechtel-Walz W
AD  - Renal Division, Department of Medicine, Medical Center, University of Freiburg, 
      Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20230713
PL  - Switzerland
TA  - Nephron
JT  - Nephron
JID - 0331777
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Antioxidants)
SB  - IM
MH  - Humans
MH  - Reactive Oxygen Species/metabolism
MH  - Antioxidants/metabolism
MH  - Kidney/metabolism
MH  - Oxidative Stress
MH  - *Renal Insufficiency, Chronic/metabolism
MH  - *Acute Kidney Injury/metabolism
MH  - Autophagy/physiology
MH  - *Kidney Failure, Chronic/metabolism
OTO - NOTNLM
OT  - Acute kidney injury
OT  - Autophagy
OT  - Chronic kidney disease
OT  - Oxidative stress
OT  - Reactive oxygen species
EDAT- 2023/07/14 13:07
MHDA- 2023/10/04 06:44
CRDT- 2023/07/13 18:23
PHST- 2022/09/08 00:00 [received]
PHST- 2023/05/19 00:00 [accepted]
PHST- 2023/10/04 06:44 [medline]
PHST- 2023/07/14 13:07 [pubmed]
PHST- 2023/07/13 18:23 [entrez]
AID - 000531290 [pii]
AID - 10.1159/000531290 [doi]
PST - ppublish
SO  - Nephron. 2023;147(10):627-642. doi: 10.1159/000531290. Epub 2023 Jul 13.