Evidence map›Paper›PMID 24483238›Full record

ReviewAntioxidants & redox signaling2014

Oxidative stress, redox signaling, and autophagy: cell death versus survival.

Juliana Navarro-Yepes, Michaela Burns, Annadurai Anandhan, Oleh Khalimonchuk, Luz Maria del Razo, Betzabet Quintanilla-Vega, Aglaia Pappa, Mihalis I Panayiotidis, Rodrigo Franco

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
199citing papers in PubMed, 2 pooled it
22.5field-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

199 citing papers in PubMed, 2 syntheses or guidelines pooled it, 418 citations in OpenAlex.

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139 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 4 countries.

Juliana Navarro-Yepes1 Redox Biology Center, University of Nebraska-Lincoln , Lincoln, Nebraska.
Michaela Burns
Annadurai Anandhan
Oleh Khalimonchuk
Luz Maria del Razo
Betzabet Quintanilla-Vega
Aglaia Pappa
Mihalis I Panayiotidis
Rodrigo Franco
University of Nebraska–Lincoln · USCentro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional · MXDemocritus University of Thrace · GRHeriot-Watt University · GB

Funding

THE REDOX-MEDIATED REGULATION OF IRON-RESPONSIVE GENE EXPRESSION IN LIVERP20RR017675 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2002 to 2011
$20.4M
Redox Biology CenterP30GM103335 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2012 to 2016
$4.3M
NCRR NIH HHS P20RR17675NIGMS NIH HHS P30 GM103335
6 · The paper itself

Abstract

significanceThe molecular machinery regulating autophagy has started becoming elucidated, and a number of studies have undertaken the task to determine the role of autophagy in cell fate determination within the context of human disease progression. Oxidative stress and redox signaling are also largely involved in the etiology of human diseases, where both survival and cell death signaling cascades have been reported to be modulated by reactive oxygen species (ROS) and reactive nitrogen species (RNS). RECENT ADVANCES: To date, there is a good understanding of the signaling events regulating autophagy, as well as the signaling processes by which alterations in redox homeostasis are transduced to the activation/regulation of signaling cascades. However, very little is known about the molecular events linking them to the regulation of autophagy. This lack of information has hampered the understanding of the role of oxidative stress and autophagy in human disease progression. CRITICAL ISSUES: In this review, we will focus on (i) the molecular mechanism by which ROS/RNS generation, redox signaling, and/or oxidative stress/damage alter autophagic flux rates; (ii) the role of autophagy as a cell death process or survival mechanism in response to oxidative stress; and (iii) alternative mechanisms by which autophagy-related signaling regulate mitochondrial function and antioxidant response. FUTURE DIRECTIONS: Our research efforts should now focus on understanding the molecular basis of events by which autophagy is fine tuned by oxidation/reduction events. This knowledge will enable us to understand the mechanisms by which oxidative stress and autophagy regulate human diseases such as cancer and neurodegenerative disorders.

Indexed as

AnimalsAutophagyCell DeathHumansOxidation-ReductionOxidative StressReactive Nitrogen SpeciesReactive Oxygen SpeciesReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID24483238
PMCPMC4048575
OpenAlexW2039531276

What OpenQuestion holds

Textmetadata
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.