Evidence map›Paper›PMID 26704446›Full record

ArticleMechanisms of ageing and development2016

Glutathione S-transferase mediates an ageing response to mitochondrial dysfunction.

Beverley M Dancy, Nicole Brockway, Renjini Ramadasan-Nair, Yoing Yang, Margaret M Sedensky, Philip G Morgan

Open access · greenAbstract read
In one paragraph

Article in Mechanisms of ageing and development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 20 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

6 authors at 3 institutions in 1 country.

Beverley M DancyCenter for Developmental Therapeutics, Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA. Electronic address: beverley.m.dancy@gmail.com.
Nicole BrockwayCenter for Developmental Therapeutics, Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA. Electronic address: nicolebrockway9@gmail.com.
Renjini Ramadasan-NairCenter for Developmental Therapeutics, Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA. Electronic address: renjini@outlook.com.
Yoing YangDepartment of Genetics, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: yyoing@gmail.com.
Margaret M SedenskyCenter for Developmental Therapeutics, Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA; Department of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, BB-1469, Seattle, WA 98195, USA. Electronic address: sedenm@u.washington.edu.
Philip G MorganCenter for Developmental Therapeutics, Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA; Department of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, BB-1469, Seattle, WA 98195, USA. Electronic address: philip.morgan@seattlechildrens.org.
Seattle Children's Hospital · USSeattle Pacific University · USCase Western Reserve University · US

Funding

Interaction of ubiquinone &complex I control longevityR01AG026073 · NIA · SEATTLE CHILDREN'S HOSPITAL · PI MORGAN, PHILIP G · 2005 to 2009
$1.5M
NIA NIH HHS R01 AG026073
6 · The paper itself

Abstract

To understand primary mitochondrial disease, we utilized a complex I-deficient Caenorhabditis elegans mutant, gas-1. These animals strongly upregulate the expression of gst-14 (encoding a glutathione S-transferase). Knockdown of gst-14 dramatically extends the lifespan of gas-1 and increases hydroxynonenal (HNE) modified mitochondrial proteins without improving complex I function. We observed no change in reactive oxygen species levels as measured by Mitosox staining, consistent with a potential role of GST-14 in HNE clearance. The upregulation of gst-14 in gas-1 animals is specific to the pharynx. These data suggest that an HNE-mediated response in the pharynx could be beneficial for lifespan extension in the context of complex I dysfunction in C. elegans. Thus, whereas HNE is typically considered damaging, our work is consistent with recent reports of its role in signaling, and that in this case, the signal is pro-longevity in a model of mitochondrial dysfunction.

Indexed as

AgingAldehydesAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDisease Models, AnimalElectron TransportGlutathione TransferaseGreen Fluorescent ProteinsMitochondriaMitochondrial DiseasesMusclesNADH DehydrogenasePharynxReactive Oxygen SpeciesRNA InterferenceAldehydesCaenorhabditis elegans ProteinsGAS-1 protein, C elegansGlutathione TransferaseGreen Fluorescent ProteinsNADH DehydrogenaseReactive Oxygen Speciestert-4-hydroxy-2-nonenalCaenorhabditis elegansGlutathione S-transferaseHydroxynonenalLongevityMitochondrial respiratory chainReactive oxygen species

Identifiers

PMID26704446
PMCPMC5178136
OpenAlexW2199170229

What OpenQuestion holds

Textmetadata
LicenceTDM
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.