Evidence map›Paper›PMID 28450391›Full record

ArticleThe Journal of biological chemistry2017

Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex III.

Paavo Korge, Guillaume Calmettes, Scott A John, James N Weiss

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023
    Review
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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.

Paavo KorgeFrom the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
Guillaume CalmettesFrom the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
Scott A JohnFrom the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
James N WeissFrom the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095 jweiss@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Mitochondrial pathways in NO induced cardioprotectionR01HL101228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA, PING, PEIPEI · 2010 to 2013
$2.6M
Hexokinases and CardioprotectionR01HL117385 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PING, PEIPEI, WEISS, JAMES N · 2013 to 2016
$1.9M
NHLBI NIH HHS R01 HL101228NHLBI NIH HHS R01 HL117385
6 · The paper itself

Abstract

Recent evidence has implicated succinate-driven reverse electron transport (RET) through complex I as a major source of damaging reactive oxygen species (ROS) underlying reperfusion injury after prolonged cardiac ischemia. However, this explanation may be incomplete, because RET on reperfusion is self-limiting and therefore transient. RET can only generate ROS when mitochondria are well polarized, and it ceases when permeability transition pores (PTP) open during reperfusion. Because prolonged ischemia/reperfusion also damages electron transport complexes, we investigated whether such damage could lead to ROS production after PTP opening has occurred. Using isolated cardiac mitochondria, we demonstrate a novel mechanism by which antimycin-inhibited complex III generates significant amounts of ROS in the presence of Mg

Indexed as

Adenosine DiphosphateAlamethicinAnimalsAntimycin ABiocatalysisCalcium SignalingElectron Transport Complex IIIEnzyme ActivationEnzyme InhibitorsHydrogen PeroxideIonophoresMagnesiumMalate DehydrogenaseMitochondria, HeartNADOxidation-ReductionAdenosine DiphosphateAlamethicinantimycinAntimycin AElectron Transport Complex IIIEnzyme InhibitorsHydrogen PeroxideIonophoresMagnesiumMalate DehydrogenaseNADpiericidin APolyenesPyridinesReactive Oxygen SpeciesstigmatellinUbiquinonecomplex IIIelectron transport system (ETS)mitochondrianicotinamide adenine dinucleotide (NADH)oxidation-reduction (redox)reactive oxygen species (ROS)

Identifiers

PMID28450391
PMCPMC5473241
OpenAlexW4249032922

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.