Evidence map›Paper›PMID 22247756›Full record

ArticlePloS one2012

Transcriptional profiling of human familial longevity indicates a role for ASF1A and IL7R.

Willemijn M Passtoors, Judith M Boer, Jelle J Goeman, Erik B van den Akker, Joris Deelen, Bas J Zwaan, Ann Scarborough, Ruud van der Breggen, Rolf H A M Vossen, Jeanine J Houwing-Duistermaat and 8 more

Erratum issuedOpen access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  10. Splicing alterations in healthy aging and disease.Wiley interdisciplinary reviews. RNA · 2021
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

18 authors at 4 institutions in 2 countries.

Willemijn M PasstoorsSection of Molecular Epidemiology, Leiden University Medical Center, Leiden, The Netherlands. w.m.passtoors@lumc.nl
Judith M Boer
Jelle J Goeman
Erik B van den Akker
Joris Deelen
Bas J Zwaan
Ann Scarborough
Ruud van der Breggen
Rolf H A M Vossen
Jeanine J Houwing-Duistermaat
Gert Jan B van Ommen
Rudi G J Westendorp
Diana van Heemst
Anton J M de Craen
Andrew J White
David A Gunn
Marian Beekman
P Eline Slagboom
Leiden University Medical Center · NLUnilever (United Kingdom) · GBLeiden University · NLNetherlands Consortium for Healthy Ageing · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Leiden Longevity Study consists of families that express extended survival across generations, decreased morbidity in middle-age, and beneficial metabolic profiles. To identify which pathways drive this complex phenotype of familial longevity and healthy aging, we performed a genome-wide gene expression study within this cohort to screen for mRNAs whose expression changes with age and associates with longevity. We first compared gene expression profiles from whole blood samples between 50 nonagenarians and 50 middle-aged controls, resulting in identification of 2,953 probes that associated with age. Next, we determined which of these probes associated with longevity by comparing the offspring of the nonagenarians (50 subjects) and the middle-aged controls. The expression of 360 probes was found to change differentially with age in members of the long-lived families. In a RT-qPCR replication experiment utilizing 312 controls, 332 offspring and 79 nonagenarians, we confirmed a nonagenarian specific expression profile for 21 genes out of 25 tested. Since only some of the offspring will have inherited the beneficial longevity profile from their long-lived parents, the contrast between offspring and controls is expected to be weak. Despite this dilution of the longevity effects, reduced expression levels of two genes, ASF1A and IL7R, involved in maintenance of chromatin structure and the immune system, associated with familial longevity already in middle-age. The size of this association increased when controls were compared to a subfraction of the offspring that had the highest probability to age healthily and become long-lived according to beneficial metabolic parameters. In conclusion, an "aging-signature" formed of 21 genes was identified, of which reduced expression of ASF1A and IL7R marked familial longevity already in middle-age. This indicates that expression changes of genes involved in metabolism, epigenetic control and immune function occur as a function of age, and some of these, like ASF1A and IL7R, represent early features of familial longevity and healthy ageing.

Indexed as

Gene Expression ProfilingGenetic Predisposition to DiseaseAdultAgedAged, 80 and overAgingBiomarkersCase-Control StudiesCell Cycle ProteinsFemaleHealth StatusHumansLongevityMaleMiddle AgedMolecular ChaperonesASF1A protein, humanBiomarkersCell Cycle ProteinsMolecular ChaperonesReceptors, Interleukin-7RNA, Messenger

Identifiers

PMID22247756
PMCPMC3256132
OpenAlexW2042213062

What OpenQuestion holds

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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.