Evidence map›Paper›PMID 24515117›Full record

ReviewThe Journal of biological chemistry2014

Role of metabolic H2O2 generation: redox signaling and oxidative stress.

Helmut Sies

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 326 papers.

0numbers the graph read from it
0cells of the map it votes in
326citing papers in PubMed
32.3field-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

326 citing papers in PubMed, 718 citations in OpenAlex.

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  6. ICSI media buffers: is there room for improvement?Journal of assisted reproduction and genetics · 2026
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266 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

1 author at 1 institution in 1 country.

Helmut SiesFrom the From the Institute of Biochemistry and Molecular Biology I, and.
Leibniz Institute of Environmental Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hydrogen peroxide, the nonradical 2-electron reduction product of oxygen, is a normal aerobic metabolite occurring at about 10 nm intracellular concentration. In liver, it is produced at 50 nmol/min/g of tissue, which is about 2% of total oxygen uptake at steady state. Metabolically generated H2O2 emerged from recent research as a central hub in redox signaling and oxidative stress. Upon generation by major sources, the NADPH oxidases or Complex III of the mitochondrial respiratory chain, H2O2 is under sophisticated fine control of peroxiredoxins and glutathione peroxidases with their backup systems as well as by catalase. Of note, H2O2 is a second messenger in insulin signaling and in several growth factor-induced signaling cascades. H2O2 transport across membranes is facilitated by aquaporins, denoted as peroxiporins. Specialized protein cysteines operate as redox switches using H2O2 as thiol oxidant, making this reactive oxygen species essential for poising the set point of the redox proteome. Major processes including proliferation, differentiation, tissue repair, inflammation, circadian rhythm, and aging use this low molecular weight oxygen metabolite as signaling compound.

Indexed as

Oxidative StressSignal TransductionAnimalsHumansHydrogen PeroxideOxidation-ReductionHydrogen PeroxideAquaporinCatalaseGlutathione PeroxidaseHydrogen PeroxideInsulinMitochondriaNADPH OxidasePeroxiredoxinRedoxSecond Messenger

Identifiers

PMID24515117
PMCPMC3979367
OpenAlexW1976087136

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.