Evidence map›Paper›PMID 25611376›Full record

ArticleCell death & disease2015

Age-related proteostasis and metabolic alterations in Caspase-2-deficient mice.

C H Wilson, S Shalini, A Filipovska, T R Richman, S Davies, S D Martin, S L McGee, J Puccini, A Nikolic, L Dorstyn and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 8% 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, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Dynamic Changes in Gene Expression Through Aging inbioRxiv : the preprint server for biology · 2024
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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

11 authors at 4 institutions in 1 country.

C H WilsonCentre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia.
S ShaliniCentre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia.
A Filipovska1] Mitochondrial Medicine and Biology Group, Harry Perkins Institute of Medical Research, Nedlands, Western Australia, Australia [2] School of Chemistry and Biochemistry, The University of Western Australia, Nedlands, Western Australia, Australia.
T R RichmanMitochondrial Medicine and Biology Group, Harry Perkins Institute of Medical Research, Nedlands, Western Australia, Australia.
S DaviesMitochondrial Medicine and Biology Group, Harry Perkins Institute of Medical Research, Nedlands, Western Australia, Australia.
S D Martin1] Metabolic Remodelling Laboratory, School of Medicine, Deakin University, Geelong, Victoria, Australia [2] Metabolism and Inflammation Program, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
S L McGee1] Metabolic Remodelling Laboratory, School of Medicine, Deakin University, Geelong, Victoria, Australia [2] Metabolism and Inflammation Program, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
J PucciniCentre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia.
A NikolicCentre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia.
L DorstynCentre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia.
S KumarCentre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia.
University of South Australia · AUHarry Perkins Institute of Medical Research · AUDeakin University · AUCentre for Cancer Biology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ageing is a complex biological process for which underlying biochemical changes are still largely unknown. We performed comparative profiling of the cellular proteome and metabolome to understand the molecular basis of ageing in Caspase-2-deficient (Casp2(-/-)) mice that are a model of premature ageing in the absence of overt disease. Age-related changes were determined in the liver and serum of young (6-9 week) and aged (18-24 month) wild-type and Casp2(-/-) mice. We identified perturbed metabolic pathways, decreased levels of ribosomal and respiratory complex proteins and altered mitochondrial function that contribute to premature ageing in the Casp2(-/-) mice. We show that the metabolic profile changes in the young Casp2(-/-) mice resemble those found in aged wild-type mice. Intriguingly, aged Casp2(-/-) mice were found to have reduced blood glucose and improved glucose tolerance. These results demonstrate an important role for caspase-2 in regulating proteome and metabolome remodelling during ageing.

Indexed as

MetabolomeAgingAmino AcidsAnimalsCaspase 2GlucoseGlucose IntoleranceHomeostasisLipid MetabolismLiverMaleMetabolomicsMiceMice, Inbred C57BLMitochondriaNADPAmino AcidsCasp2 protein, mouseCaspase 2GlucoseNADPProteome

Identifiers

PMID25611376
PMCPMC4669765
OpenAlexW2005273772

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.