Evidence map›Paper›PMID 31382550›Full record

ReviewInternational journal of molecular sciences2019

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

Gur P Kaushal, Kiran Chandrashekar, Luis A Juncos

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
12.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. A Novel Role of Ume6 inJournal of fungi (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Short-Term Intake ofAntioxidants (Basel, Switzerland) · 2025
    Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Chemical Constituents from the Fruit ofAntioxidants (Basel, Switzerland) · 2024
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Gur P Kaushal4301 West Markham, Slot 501, Little Rock, AR 72205, USA. Kaushalgurp@uams.edu.
Kiran ChandrashekarRenal 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.
Luis A JuncosRenal 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.ORCID 0000-0002-4630-2747
Central Arkansas Veterans Healthcare System · US

Funding

U.S. Department of Veterans Affairs BX000444
6 · The paper itself

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.

Indexed as

Acute Kidney InjuryAMP-Activated Protein Kinase KinasesAutophagyAutophagy-Related Protein-1 HomologHumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1Mechanistic Target of Rapamycin Complex 1NF-E2-Related Factor 2Oxidative StressProtein KinasesReactive Oxygen SpeciesRenal Insufficiency, ChronicRNA-Binding ProteinsAMP-Activated Protein Kinase KinasesAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Mechanistic Target of Rapamycin Complex 1NFE2L2 protein, humanNF-E2-Related Factor 2P62 protein, humanProtein KinasesReactive Oxygen SpeciesRNA-Binding ProteinsULK1 protein, humanacute kidney injuryAMPKautophagychronic kidney diseasediabetic nephropathymTORC1oxidantsreactive oxygen species

Identifiers

PMID31382550
PMCPMC6696055
OpenAlexW2964793689

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.