Evidence map›Paper›PMID 26184557›Full record

ReviewRedox biology2015

Redox regulation of FoxO transcription factors.

Lars-Oliver Klotz, Cristina Sánchez-Ramos, Ignacio Prieto-Arroyo, Pavel Urbánek, Holger Steinbrenner, Maria Monsalve

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 380 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
380citing papers in PubMed, 2 pooled it
20.5field-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

380 citing papers in PubMed, 2 syntheses or guidelines pooled it, 725 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Thioredoxin-2 Alleviates Osteoporosis by Restraining FOXO3a Nuclear Translocation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Life (Basel, Switzerland) · 2026
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320 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

6 authors at 2 institutions in 2 countries.

Lars-Oliver KlotzInstitute of Nutrition, Department of Nutrigenomics, Friedrich-Schiller-Universität Jena, Dornburger Straße 29, 07743 Jena, Germany. Electronic address: lars-oliver.klotz@uni-jena.de.
Cristina Sánchez-RamosInstituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), Arturo Duperier, 4, 28029 Madrid, Spain.
Ignacio Prieto-ArroyoInstituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), Arturo Duperier, 4, 28029 Madrid, Spain.
Pavel UrbánekInstitute of Nutrition, Department of Nutrigenomics, Friedrich-Schiller-Universität Jena, Dornburger Straße 29, 07743 Jena, Germany.
Holger SteinbrennerInstitute of Nutrition, Department of Nutrigenomics, Friedrich-Schiller-Universität Jena, Dornburger Straße 29, 07743 Jena, Germany.
Maria MonsalveInstituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), Arturo Duperier, 4, 28029 Madrid, Spain. Electronic address: mpmonsalve@iib.uam.es.
Friedrich Schiller University Jena · DEUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factors of the forkhead box, class O (FoxO) family are important regulators of the cellular stress response and promote the cellular antioxidant defense. On one hand, FoxOs stimulate the transcription of genes coding for antioxidant proteins located in different subcellular compartments, such as in mitochondria (i.e. superoxide dismutase-2, peroxiredoxins 3 and 5) and peroxisomes (catalase), as well as for antioxidant proteins found extracellularly in plasma (e.g., selenoprotein P and ceruloplasmin). On the other hand, reactive oxygen species (ROS) as well as other stressful stimuli that elicit the formation of ROS, may modulate FoxO activity at multiple levels, including posttranslational modifications of FoxOs (such as phosphorylation and acetylation), interaction with coregulators, alterations in FoxO subcellular localization, protein synthesis and stability. Moreover, transcriptional and posttranscriptional control of the expression of genes coding for FoxOs is sensitive to ROS. Here, we review these aspects of FoxO biology focusing on redox regulation of FoxO signaling, and with emphasis on the interplay between ROS and FoxOs under various physiological and pathophysiological conditions. Of particular interest are the dual role played by FoxOs in cancer development and their key role in whole body nutrient homeostasis, modulating metabolic adaptations and/or disturbances in response to low vs. high nutrient intake. Examples discussed here include calorie restriction and starvation as well as adipogenesis, obesity and type 2 diabetes.

Indexed as

Amino Acid SequenceBlood ProteinsDiabetes Mellitus, Type 2Forkhead Box Protein O1Forkhead Transcription FactorsGene Expression RegulationHumansMitochondrial ProteinsMolecular Sequence DataNeoplasmsObesityOxidation-ReductionOxidative StressProtein IsoformsProtein Structure, TertiaryReactive Oxygen SpeciesBlood ProteinsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanMitochondrial ProteinsProtein IsoformsReactive Oxygen SpeciesAktAntioxidant proteinsC. elegansDAF-16Forkhead box proteinsInsulin signalingOxidative stressStress signaling

Identifiers

PMID26184557
PMCPMC4511623
OpenAlexW1820314031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.