Evidence map›Paper›PMID 33319867›Full record

ArticleCommunications biology2020

NAD

Xuegang Yuan, Yijun Liu, Brent M Bijonowski, Ang-Chen Tsai, Qin Fu, Timothy M Logan, Teng Ma, Yan Li

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
4.6field-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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Mitochondria-Targeting Moieties Based on N-Tethered Pyridinium Cations.Angewandte Chemie (International ed. in English) · 2026
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  14. Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025
    Review
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  17. The role of NADnpj metabolic health and disease · 2025
    Review
  18. Article
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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

8 authors at 4 institutions in 2 countries.

Xuegang YuanDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. xy13b@my.fsu.edu.
Yijun LiuDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA.
Brent M BijonowskiDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA.
Ang-Chen TsaiDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA.
Qin FuDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA.
Timothy M LoganDepartment of Chemistry and Biochemistry, Florida State University, Tallahassee, FL, USA.
Teng MaDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA.
Yan LiDepartment of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. yli4@fsu.edu.
Florida A&M University - Florida State University College of Engineering · USCornell University · USFlorida State University · USUniversity of Florida · US

Funding

MR Analysis of Pre-Conditioned Human Mesenchymal Stem Cells for Stroke TherapyR01NS102395 · NINDS · FLORIDA STATE UNIVERSITY · PI GRANT, SAMUEL COLLES · 2017 to 2021
$1.7M
NINDS NIH HHS R01 NS102395
6 · The paper itself

Abstract

Human mesenchymal stem cells (hMSCs) promote endogenous tissue regeneration and have become a promising candidate for cell therapy. However, in vitro culture expansion of hMSCs induces a rapid decline of stem cell properties through replicative senescence. Here, we characterize metabolic profiles of hMSCs during expansion. We show that alterations of cellular nicotinamide adenine dinucleotide (NAD + /NADH) redox balance and activity of the Sirtuin (Sirt) family enzymes regulate cellular senescence of hMSCs. Treatment with NAD + precursor nicotinamide increases the intracellular NAD + level and re-balances the NAD + /NADH ratio, with enhanced Sirt-1 activity in hMSCs at high passage, partially restores mitochondrial fitness and rejuvenates senescent hMSCs. By contrast, human fibroblasts exhibit limited senescence as their cellular NAD + /NADH balance is comparatively stable during expansion. These results indicate a potential metabolic and redox connection to replicative senescence in adult stem cells and identify NAD + as a metabolic regulator that distinguishes stem cells from mature cells. This study also suggests potential strategies to maintain cellular homeostasis of hMSCs in clinical applications.

Indexed as

Cellular SenescenceEnergy MetabolismOxidation-ReductionCell ProliferationCells, CulturedFibroblastsHumansMesenchymal Stem CellsMitochondriaNADRejuvenationNAD

Identifiers

PMID33319867
PMCPMC7738682
OpenAlexW3111851840

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.