Evidence map›Paper›PMID 33316776›Full record

ArticleAging2020

Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism.

Qun-Yan Xiang, Feng Tian, Xiao Du, Jin Xu, Li-Yuan Zhu, Li-Ling Guo, Tie Wen, You-Shuo Liu, Ling Liu

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  9. Observational
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  12. New insight into dyslipidemia-induced cellular senescence in atherosclerosis.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
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  14. Review
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

9 authors at 3 institutions in 1 country.

Qun-Yan XiangDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Feng TianDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Xiao DuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Jin XuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Li-Yuan ZhuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Li-Ling GuoDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Tie WenDepartment of Emergency Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
You-Shuo LiuDepartment of Geriatrics, Institute of Aging and Geriatrics, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Ling LiuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, PR China.
Second Xiangya Hospital of Central South University · CNHunan Provincial Center for Disease Control and Prevention · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of senescent adipose-derived mesenchymal stem cells (AMSCs) in subcutaneous white adipose tissue (WAT) is the main cause for the deterioration of WAT and the subsequent age-related disorders in obesity. The number of AMSCs staining positively for senescence-associated-β-galactosidase (SA-β-Gal) increased significantly after incubation with postprandial triglyceride-rich lipoproteins (TRL), accompanied by an impaired cell proliferation capacity and increased expression of inflammatory factors. Besides, the expression of anti-aging protein, silent mating-type information regulation 2 homolog 1 (SIRT1), was downregulated significantly, while those of acetylated p53 (Ac-p53), total p53, and p21 proteins were upregulated significantly during postprandial TRL-induced premature senescence of AMSCs. Furthermore, the production of intracellular reactive oxygen species (ROS) in the TRL group increased significantly, while pretreatment with the ROS scavenger N-acetyl-L-cysteine effectively attenuated the premature senescence of AMSCs by decreasing ROS production and upregulating SIRT1 level. Thus, postprandial TRL induced premature senescence of AMSCs through the SIRT1/p53/Ac-p53/p21 axis, partly through increased oxidative stress.

Indexed as

Cellular SenescenceAcetylationAcetylcysteineAdipogenesisAnimalsbeta-GalactosidaseCell ProliferationCyclin-Dependent Kinase Inhibitor p21Down-RegulationInflammationLipoproteinsMesenchymal Stem CellsMiceObesityOxidative StressPostprandial PeriodAcetylcysteinebeta-GalactosidaseCyclin-Dependent Kinase Inhibitor p21LipoproteinsReactive Oxygen SpeciesSirt1 protein, mouseSirtuin 1TriglyceridesTrp53 protein, mouseTumor Suppressor Protein p53adipose-derived mesenchymal stem cellsoxidative stresspremature senescenceSIRT1triglyceride-rich lipoproteins

Identifiers

PMID33316776
PMCPMC7803527
OpenAlexW3113145905

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.