Evidence map›Paper›PMID 29717979›Full record

ArticleeLife2018

Boosting ATM activity alleviates aging and extends lifespan in a mouse model of progeria.

Minxian Qian, Zuojun Liu, Linyuan Peng, Xiaolong Tang, Fanbiao Meng, Ying Ao, Mingyan Zhou, Ming Wang, Xinyue Cao, Baoming Qin and 6 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 78 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

16 authors at 5 institutions in 2 countries.

Minxian Qian *Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.ORCID http://orcid.org/0000-0002-1763-2325
Zuojun Liu *Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Linyuan PengGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Xiaolong TangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.ORCID http://orcid.org/0000-0002-4744-5846
Fanbiao MengGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Ying AoGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Mingyan ZhouGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Ming WangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Xinyue CaoGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Baoming QinSouth China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Zimei WangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.
Zhongjun ZhouSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.ORCID http://orcid.org/0000-0001-7092-8128
Guangming WangEast Hospital, Tongji University School of Medicine, Shanghai, China.
Zhengliang GaoShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Jun XuEast Hospital, Tongji University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-8565-1723
Baohua LiuGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Shenzhen, China.ORCID http://orcid.org/0000-0002-1599-8059
Shenzhen University Health Science Center · CNChinese Academy of Sciences · CNTongji University · CNShanghai East Hospital · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage accumulates with age (Lombard et al., 2005). However, whether and how robust DNA repair machinery promotes longevity is elusive. Here, we demonstrate that ATM-centered DNA damage response (DDR) progressively declines with senescence and age, while low dose of chloroquine (CQ) activates ATM, promotes DNA damage clearance, rescues age-related metabolic shift, and prolongs replicative lifespan. Molecularly, ATM phosphorylates SIRT6 deacetylase and thus prevents MDM2-mediated ubiquitination and proteasomal degradation. Extra copies of

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCaenorhabditis elegansChloroquineDNA RepairLongevityMiceMice, KnockoutMotor ActivityPhosphorylationProgeriaProtein Processing, Post-TranslationalProteolysisProto-Oncogene Proteins c-mdm2SirtuinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseChloroquineMdm2 protein, mouseProto-Oncogene Proteins c-mdm2Sirt6 protein, mouseSirtuinsageingATMbiochemistrychemical biologychromosomesgene expressiongenome stabilitymouseSIRT6

Identifiers

PMID29717979
PMCPMC5957528
OpenAlexW2801799722

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.