Evidence map›Paper›PMID 27171124›Full record

ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2016

Revisiting Kadenbach: Electron flux rate through cytochrome c-oxidase determines the ATP-inhibitory effect and subsequent production of ROS.

Sebastian Vogt, Annika Rhiel, Petra Weber, Rabia Ramzan

Open access · hybridAbstract readReview
In one paragraph

Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Sebastian VogtCardiovascular Research Lab, Biochemical Pharmacological Research Center, Philipps-University Marburg, Marburg, Germany.
Annika RhielCardiovascular Research Lab, Biochemical Pharmacological Research Center, Philipps-University Marburg, Marburg, Germany.
Petra WeberCardiovascular Research Lab, Biochemical Pharmacological Research Center, Philipps-University Marburg, Marburg, Germany.
Rabia RamzanCardiovascular Research Lab, Biochemical Pharmacological Research Center, Philipps-University Marburg, Marburg, Germany.
Philipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial respiration is the predominant source of ATP. Excessive rates of electron transport cause a higher production of harmful reactive oxygen species (ROS). There are two regulatory mechanisms known. The first, according to Mitchel, is dependent on the mitochondrial membrane potential that drives ATP synthase for ATP production, and the second, the Kadenbach mechanism, is focussed on the binding of ATP to Cytochrome c Oxidase (CytOx) at high ATP/ADP ratios, which results in an allosteric conformational change to CytOx, causing inhibition. In times of stress, ATP-dependent inhibition is switched off and the activity of CytOx is exclusively determined by the membrane potential, leading to an increase in ROS production. The second mechanism for respiratory control depends on the quantity of electron transfer to the Heme aa3 of CytOx. When ATP is bound to CytOx the enzyme is inhibited, and ROS formation is decreased, although the mitochondrial membrane potential is increased.

Indexed as

Adenosine TriphosphateAllosteric RegulationAnimalsElectron TransportElectron Transport Complex IVHumansKineticsMembrane Potential, MitochondrialMitochondriaMitochondrial Proton-Translocating ATPasesReactive Oxygen SpeciesAdenosine TriphosphateElectron Transport Complex IVMitochondrial Proton-Translocating ATPasesReactive Oxygen Speciesallosteric inhibitioncytochrome c oxidaseenzyme kineticsischaemic preconditioningphosphodiesterase inhibitorsreactive oxygen species

Identifiers

PMID27171124
PMCPMC5084804
OpenAlexW2353664621

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.