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Molecular Interactions Between Reactive Oxygen Species and Autophagy in Kidney Disease.

Authors
  • Kaushal, Gur P1, 2
  • Chandrashekar, Kiran3
  • Juncos, Luis A3
  • 1 4301 West Markham, Slot 501, Little Rock, AR 72205, USA. [email protected]
  • 2 Renal Section, Central Arkansas Veterans Healthcare System Little Rock, Arkansas and Division of Nephrology, Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. [email protected]
  • 3 Renal Section, Central Arkansas Veterans Healthcare System Little Rock, Arkansas and Division of Nephrology, Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Aug 03, 2019
Volume
20
Issue
15
Identifiers
DOI: 10.3390/ijms20153791
PMID: 31382550
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Reactive oxygen species (ROS) are highly reactive signaling molecules that maintain redox homeostasis in mammalian cells. Dysregulation of redox homeostasis under pathological conditions results in excessive generation of ROS, culminating in oxidative stress and the associated oxidative damage of cellular components. ROS and oxidative stress play a vital role in the pathogenesis of acute kidney injury and chronic kidney disease, and it is well documented that increased oxidative stress in patients enhances the progression of renal diseases. Oxidative stress activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular oxidized and damaged macromolecules and dysfunctional organelles. In this review, we report the current understanding of the molecular regulation of autophagy in response to oxidative stress in general and in the pathogenesis of kidney diseases. We summarize how the molecular interactions between ROS and autophagy involve ROS-mediated activation of autophagy and autophagy-mediated reduction of oxidative stress. In particular, we describe how ROS impact various signaling pathways of autophagy, including mTORC1-ULK1, AMPK-mTORC1-ULK1, and Keap1-Nrf2-p62, as well as selective autophagy including mitophagy and pexophagy. Precise elucidation of the molecular mechanisms of interactions between ROS and autophagy in the pathogenesis of renal diseases may identify novel targets for development of drugs for preventing renal injury.

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