Evidence map›Paper›PMID 31782607›Full record

ArticleAging cell2020

Base excision repair but not DNA double-strand break repair is impaired in aged human adipose-derived stem cells.

Haiping Zhang, Bailian Cai, Anke Geng, Huanyin Tang, Wenjun Zhang, Sheng Li, Ying Jiang, Rong Tan, Xiaoping Wan, Zhiyong Mao

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Biomarkers of aging.Science China. Life sciences · 2023
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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

10 authors at 4 institutions in 1 country.

Haiping ZhangClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Bailian CaiClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Anke GengClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Huanyin TangClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Wenjun ZhangDepartment of Plastic Surgery, Changzheng Hospital, Shanghai, China.
Sheng LiClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Ying JiangClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Rong TanCenter for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Xiaoping WanClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Zhiyong MaoClinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.ORCID 0000-0002-5298-1918
Shanghai First Maternity and Infant Hospital · CNCentral South University · CNChina Pharmaceutical University · CNShanghai Changzheng Hospital · CN

Funding

Fundamental Research Funds for the Central Universities, the Open Project Program of State Key Laboratory of Natural Medicines SKLNMKF201905National Key R&D Program of China 2017YFA0103300National Key R&D Program of China 2018YFC2000100National Science Foundation of China 31570813National Science Foundation of China 31871438National Science Foundation of China 81601212National Science Foundation of China 81622019National Science Foundation of China 81702638National Science Foundation of China 81702770Program of Shanghai Academic Research Leader 19XD1403000Shanghai municipal medical and health discipline construction projects 2017ZZ02015"Shu Guang" project supported by Shanghai Municipal Education Commission and Shanghai Education Development Foundation 19SG18
6 · The paper itself

Abstract

The decline in DNA repair capacity contributes to the age-associated decrease in genome integrity in somatic cells of different species. However, due to the lack of clinical samples and appropriate tools for studying DNA repair, whether and how age-associated changes in DNA repair result in a loss of genome integrity of human adult stem cells remains incompletely characterized. Here, we isolated 20 eyelid adipose-derived stem cell (ADSC) lines from healthy individuals (young: 10 donors with ages ranging 17-25 years; old: 10 donors with ages ranging 50-59 years). Using these cell lines, we systematically compared the efficiency of base excision repair (BER) and two DNA double-strand break (DSB) repair pathways-nonhomologous end joining (NHEJ) and homologous recombination (HR)-between the young and old groups. Surprisingly, we found that the efficiency of BER but not NHEJ or HR is impaired in aged human ADSCs, which is in contrast to previous findings that DSB repair declines with age in human fibroblasts. We also demonstrated that BER efficiency is negatively associated with tail moment, which reflects a loss of genome integrity in human ADSCs. Mechanistic studies indicated that at the protein level XRCC1, but not other BER factors, exhibited age-associated decline. Overexpression of XRCC1 reversed the decline of BER efficiency and genome integrity, indicating that XRCC1 is a potential therapeutic target for stabilizing genomes in aged ADSCs.

Indexed as

DNA Breaks, Double-StrandedAdipose TissueAdultAgingDNA End-Joining RepairDNA RepairHumansMiddle AgedRecombinational DNA RepairStem CellsUp-RegulationX-ray Repair Cross Complementing Protein 1Young AdultX-ray Repair Cross Complementing Protein 1XRCC1 protein, humanadipose-derived stem cellsbase excision repairgenome integrityhuman agingXRCC1

Identifiers

PMID31782607
PMCPMC6996963
OpenAlexW2990737143

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.