Evidence map›Paper›PMID 25607651›Full record

ArticleCell cycle (Georgetown, Tex.)2015

SIRT6 rescues the age related decline in base excision repair in a PARP1-dependent manner.

Zhu Xu, Lei Zhang, Wenjun Zhang, Du Meng, Hongxia Zhang, Ying Jiang, Xiaojun Xu, Michael Van Meter, Andrei Seluanov, Vera Gorbunova and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
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  13. NADHeliyon · 2023
    Review
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  18. Review
  19. Biomarkers of aging.Science China. Life sciences · 2023
    Review
  20. Review

13 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Zhu Xua Department of Clinical Laboratory Medicine; Shanghai Tenth People's Hospital; School of Life Sciences and Technology; Tongji University ; Shanghai , China.
Lei Zhang
Wenjun Zhang
Du Meng
Hongxia Zhang
Ying Jiang
Xiaojun Xu
Michael Van Meter
Andrei Seluanov
Vera Gorbunova
Zhiyong Mao
Shanghai Tenth People's Hospital · CNUniversity of Rochester · USTongji University · CNChina Pharmaceutical University · CNState Key Laboratory of Natural Medicine

Funding

The role of hyaluronan in longevity and cancer resistance of longest-lived rodentP01AG047200 · NIA · UNIVERSITY OF ROCHESTER · PI Vera Gorbunova · 2014 to 2026
$36.9M
The role of SIRT6 posttranslational modifications in aging and genome stability. Supplement: Testing SIRT6 activators as potential Alzheimer's disease therapy.R01AG027237 · NIA · UNIVERSITY OF ROCHESTER · PI Vera Gorbunova · 2006 to 2026
$6.2M
Molecular mechanisms which regulate SIRT6 activity and their relevance to agingF31AG041603 · NIA · UNIVERSITY OF ROCHESTER · PI VAN METER, MICHAEL JAMES · 2011 to 2014
$169k
NIA NIH HHS F31 AG041603NIA NIH HHS P01 AG047200NIA NIH HHS R01 AG027237
6 · The paper itself

Abstract

In principle, a decline in base excision repair (BER) efficiency with age should lead to genomic instability and ultimately contribute to the onset of the aging phenotype. Although multiple studies have indicated a negative link between aging and BER, the change of BER efficiency with age in humans has not been systematically analyzed. Here, with foreskin fibroblasts isolated from 19 donors between 20 and 64 y of age, we report a significant decline of BER efficiency with age using a newly developed GFP reactivation assay. We further observed a very strong negative correlation between age and the expression levels of SIRT6, a factor which is known to maintain genomic integrity by improving DNA double strand break (DSB) repair. Our mechanistic study suggests that, similar to the regulatory role that SIRT6 plays in DNA DSB repair, SIRT6 regulates BER in a PARP1-depdendent manner. Moreover, overexpression of SIRT6 rescues the decline of BER in aged fibroblasts. In summary, our results uncovered the regulatory mechanisms of BER by SIRT6, suggesting that SIRT6 reactivation in aging tissues may help delay the process of aging through improving BER.

Indexed as

DNA RepairAdultAgingCells, CulturedDNA Breaks, Double-StrandedFibroblastsForeskinGenomic InstabilityHumansLightMaleMiddle AgedPhenanthrenesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesRNA InterferenceN-(oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide hydrochloridePhenanthrenesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesRNA, Small InterferingSIRT6 protein, humanSirtuinsagingbase excision repairmono-ADP-ribosylationPARP1SIRT6SIRTUIN

Identifiers

PMID25607651
PMCPMC4614943
OpenAlexW1973327581

What OpenQuestion holds

Textmetadata
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.