Evidence map›Paper›PMID 29579719›Full record

ArticleRedox biology2018

Copper accumulation in senescent cells: Interplay between copper transporters and impaired autophagy.

Shashank Masaldan, Sharnel A S Clatworthy, Cristina Gamell, Zoe M Smith, Paul S Francis, Delphine Denoyer, Peter M Meggyesy, Sharon La Fontaine, Michael A Cater

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 78 citations in OpenAlex.

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  4. From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

9 authors at 2 institutions in 1 country.

Shashank MasaldanCentre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, Victoria 3125, Australia; The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria 3052, Australia. Electronic address: shashank.masaldan@florey.edu.au.
Sharnel A S ClatworthyCentre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, Victoria 3125, Australia.
Cristina GamellPeter MacCallum Cancer Centre, Melbourne, Victoria 3000, Australia.
Zoe M SmithSchool of Life and Environmental Sciences, Deakin University, Geelong, Victoria 3220, Australia.
Paul S FrancisSchool of Life and Environmental Sciences, Deakin University, Geelong, Victoria 3220, Australia.
Delphine DenoyerCentre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, Victoria 3125, Australia.
Peter M MeggyesyCentre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, Victoria 3125, Australia.
Sharon La FontaineCentre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, Victoria 3125, Australia; The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria 3052, Australia.
Michael A CaterCentre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, Victoria 3125, Australia; Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: mcater@deakin.edu.au.
Deakin University · AUPeter MacCallum Cancer Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is characterized by irreversible growth arrest incurred through either replicative exhaustion or by pro-oncogenic cellular stressors (radioactivity, oxidative stress, oncogenic activation). The enrichment of senescent cells in tissues with age has been associated with tissue dyshomeostasis and age-related pathologies including cancers, neurodegenerative disorders (e.g. Alzheimer's, Parkinson's, etc.) and metabolic disorders (e.g. diabetes). We identified copper accumulation as being a universal feature of senescent cells [mouse embryonic fibroblasts (MEF), human prostate epithelial cells and human diploid fibroblasts] in vitro. Elevated copper in senescent MEFs was accompanied by elevated levels of high-affinity copper uptake protein 1 (Ctr1), diminished levels of copper-transporting ATPase 1 (Atp7a) (copper export) and enhanced antioxidant defence reflected by elevated levels of glutathione (GSH), superoxide dismutase 1 (SOD1) and glutaredoxin 1 (Grx1). The levels of intracellular copper were further increased in senescent MEFs cultured in copper supplemented medium and in senescent Mottled Brindled (Mo

Indexed as

AnimalsAutophagyCation Transport ProteinsCellular SenescenceCopperCopper Transporter 1Copper-Transporting ATPasesEpithelial CellsFibroblastsGlutaredoxinsGlutathioneHomeostasisHumansLysosomesMaleMiceCation Transport ProteinsCopperCopper Transporter 1Copper-Transporting ATPasesGlrx protein, mouseGlutaredoxinsGlutathioneSLC31A1 protein, humanSuperoxide Dismutase-1AgeingAutophagyCopperHomeostasisSenescence

Identifiers

PMID29579719
PMCPMC5953000
OpenAlexW2790011736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.