Evidence map›Paper›PMID 32146156›Full record

ArticleRedox biology2020

Mitochondrial complex I derived ROS regulate stress adaptation in Drosophila melanogaster.

Filippo Scialò, Ashwin Sriram, Rhoda Stefanatos, Ruth V Spriggs, Samantha H Y Loh, L Miguel Martins, Alberto Sanz

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

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  6. Medicine on the menu: When illness informs appetite.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

7 authors at 4 institutions in 1 country.

Filippo ScialòInstitute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, United Kingdom; Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, G12 8QQ, Glasgow, United Kingdom. Electronic address: Filippo.Scialo@glasgow.ac.uk.
Ashwin SriramInstitute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, United Kingdom.
Rhoda StefanatosInstitute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, United Kingdom.
Ruth V SpriggsMRC Toxicology Unit, University of Cambridge, Hodgkin Building, Lancaster Road, Leicester, LE1 9HN, United Kingdom.
Samantha H Y LohMRC Toxicology Unit, University of Cambridge, Hodgkin Building, Lancaster Road, Leicester, LE1 9HN, United Kingdom.
L Miguel MartinsMRC Toxicology Unit, University of Cambridge, Hodgkin Building, Lancaster Road, Leicester, LE1 9HN, United Kingdom.
Alberto SanzInstitute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, United Kingdom; Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, G12 8QQ, Glasgow, United Kingdom. Electronic address: Alberto.SanzMontero@glasgow.ac.uk.
Newcastle University · GBUniversity of Cambridge · GBUniversity of Glasgow · GBMRC Toxicology Unit · GB

Funding

Medical Research Council MC_U132674518Medical Research Council MC_UU_00025/3Wellcome Trust 204715/Z/16/ZWellcome Trust 212241/Z/18/Z
6 · The paper itself

Abstract

Reactive Oxygen Species (ROS) are essential cellular messengers required for cellular homeostasis and regulate the lifespan of several animal species. The main site of ROS production is the mitochondrion, and within it, respiratory complex I (CI) is the main ROS generator. ROS produced by CI trigger several physiological responses that are essential for the survival of neurons, cardiomyocytes and macrophages. Here, we show that CI produces ROS when electrons flow in either the forward (Forward Electron Transport, FET) or reverse direction (Reverse Electron Transport, RET). We demonstrate that ROS production via RET (ROS-RET) is activated under thermal stress conditions and that interruption of ROS-RET production, through ectopic expression of the alternative oxidase AOX, attenuates the activation of pro-survival pathways in response to stress. Accordingly, we find that both suppressing ROS-RET signalling or decreasing levels of mitochondrial H

Indexed as

Drosophila melanogasterElectron Transport Complex IAnimalsElectron TransportHydrogen PeroxideReactive Oxygen SpeciesElectron Transport Complex IHydrogen PeroxideReactive Oxygen SpeciesAlternative oxidaseAOXComplex IHeat stressReactive oxygen speciesReverse electron transport

Identifiers

PMID32146156
PMCPMC7264463
OpenAlexW3004426864

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.