Evidence map›Paper›PMID 30731114›Full record

ArticleFree radical biology & medicine2019

Selective mitochondrial superoxide generation in vivo is cardioprotective through hormesis.

Salvatore Antonucci, John F Mulvey, Nils Burger, Moises Di Sante, Andrew R Hall, Elizabeth C Hinchy, Stuart T Caldwell, Anja V Gruszczyk, Soni Deshwal, Richard C Hartley and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 41 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

14 authors at 4 institutions in 2 countries.

Salvatore AntonucciDepartment of Biomedical Sciences, University of Padova, 35131, Padova, Italy.
John F MulveyDepartment of Medicine, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.
Nils BurgerMitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.
Moises Di SanteDepartment of Biomedical Sciences, University of Padova, 35131, Padova, Italy.
Andrew R HallMitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.
Elizabeth C HinchyMitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.
Stuart T CaldwellSchool of Chemistry, University of Glasgow, Glasgow, G12 8QQ, UK.
Anja V GruszczykMitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.
Soni DeshwalDepartment of Biomedical Sciences, University of Padova, 35131, Padova, Italy.
Richard C HartleySchool of Chemistry, University of Glasgow, Glasgow, G12 8QQ, UK.
Nina KaludercicNeuroscience Institute, National Research Council of Italy (CNR), 35131, Padova, Italy.
Michael P MurphyMitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.
Fabio Di LisaDepartment of Biomedical Sciences, University of Padova, 35131, Padova, Italy; Neuroscience Institute, National Research Council of Italy (CNR), 35131, Padova, Italy. Electronic address: dilisa@bio.unipd.it.
Thomas KriegDepartment of Medicine, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK. Electronic address: tk382@medschl.cam.ac.uk.
University of Cambridge · GBUniversity of Padua · ITUniversity of Glasgow · GBNeuroscience Institute · IT

Funding

Medical Research Council MC_UU_00015/3Medical Research Council MR/P000320/1Wellcome Trust 110158/Z/15/Z
6 · The paper itself

Abstract

Reactive oxygen species (ROS) have an equivocal role in myocardial ischaemia reperfusion injury. Within the cardiomyocyte, mitochondria are both a major source and target of ROS. We evaluate the effects of a selective, dose-dependent increase in mitochondrial ROS levels on cardiac physiology using the mitochondria-targeted redox cycler MitoParaquat (MitoPQ). Low levels of ROS decrease the susceptibility of neonatal rat ventricular myocytes (NRVMs) to anoxia/reoxygenation injury and also cause profound protection in an in vivo mouse model of ischaemia/reperfusion. However higher doses of MitoPQ resulted in a progressive alteration of intracellular [Ca

Indexed as

Disease Models, AnimalHormesisAnimalsAnimals, NewbornApoptosisHerbicidesMaleMiceMice, Inbred C57BLMitochondria, HeartMyocardial Reperfusion InjuryMyocytes, CardiacParaquatRatsRats, WistarSuperoxidesHerbicidesParaquatSuperoxides

Identifiers

PMID30731114
PMCPMC6607027
OpenAlexW2912853526

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.