Evidence map›Paper›PMID 29166598›Full record

ArticleCell reports2017

Biological Significance of the Suppression of Oxidative Phosphorylation in Induced Pluripotent Stem Cells.

Cheng Zhang, Maria Skamagki, Zhong Liu, Aparna Ananthanarayanan, Rui Zhao, Hu Li, Kitai Kim

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Genes as Genome Stabilizers in Pluripotent Stem Cells.Advances in experimental medicine and biology · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. International journal of molecular sciences · 2022
    Article
  10. Review
  11. Epigenetic Alterations under Oxidative Stress in Stem Cells.Oxidative medicine and cellular longevity · 2022
    Review
  12. Regulation of energy metabolism in human pluripotent stem cells.Cellular and molecular life sciences : CMLS · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

7 authors at 4 institutions in 1 country.

Cheng ZhangDepartment of Molecular Pharmacology & Experimental Therapeutics, Center for Individualized Medicine, Mayo Clinic College of Medicine, Rochester, MN 55902, USA.
Maria SkamagkiCancer Biology and Genetics Program, The Center for Cell Engineering, The Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute for Cancer Research, New York, NY 10065, USA; Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, NY 10065, USA.
Zhong LiuDepartment of Biochemistry and Molecular Genetics, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Aparna AnanthanarayananCancer Biology and Genetics Program, The Center for Cell Engineering, The Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute for Cancer Research, New York, NY 10065, USA; Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, NY 10065, USA.
Rui ZhaoDepartment of Biochemistry and Molecular Genetics, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA. Electronic address: ruizhao@uab.edu.
Hu LiDepartment of Molecular Pharmacology & Experimental Therapeutics, Center for Individualized Medicine, Mayo Clinic College of Medicine, Rochester, MN 55902, USA. Electronic address: li.hu@mayo.edu.
Kitai KimCancer Biology and Genetics Program, The Center for Cell Engineering, The Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute for Cancer Research, New York, NY 10065, USA; Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, NY 10065, USA. Electronic address: kimk@mskcc.org.
Mayo Clinic · USMemorial Sloan Kettering Cancer Center · USUniversity of Alabama at Birmingham · USCornell University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
A new hypothesis: role of p53 inhibitory factors in cellular reprogrammingR01AG043531 · NIA · SLOAN-KETTERING INST CAN RESEARCH · PI KIM, KITAI · 2014 to 2018
$2.3M
A network platform to connect drug response and prognosis phenotypes for cancersR01CA196631 · NCI · MAYO CLINIC ROCHESTER · PI LI, HU · 2016 to 2018
$1.2M
Hematopoietic potential of histocompatible embryonic stem cell linesR00HL093212 · NHLBI · SLOAN-KETTERING INST CAN RESEARCH · PI KIM, KITAI · 2012 to 2014
$717k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA196631NHLBI NIH HHS R00 HL093212NIA NIH HHS R01 AG043531
6 · The paper itself

Abstract

We discovered that induced pluripotent stem cell (iPSC) clones generated from aged tissue donors (A-iPSCs) fail to suppress oxidative phosphorylation. Compared to embryonic stem cells (ESCs) and iPSCs generated from young donors (Y-iPSCs), A-iPSCs show poor expression of the pluripotent stem cell-specific glucose transporter 3 (GLUT3) and impaired glucose uptake, making them unable to support the high glucose demands of glycolysis. Persistent oxidative phosphorylation in A-iPSCs generates higher levels of reactive oxygen species (ROS), which leads to excessive elevation of glutathione (a ROS-scavenging metabolite) and a blunted DNA damage response. These phenotypes were recapitulated in Y-iPSCs by inhibiting pyruvate dehydrogenase kinase (PDK) or supplying citrate to activate oxidative phosphorylation. In addition, oxidative phosphorylation in A-iPSC clones depletes citrate, a nuclear source of acetyl group donors for histone acetylation; this consequently alters histone acetylation status. Expression of GLUT3 in A-iPSCs recovers the metabolic defect, DNA damage response, and histone acetylation status.

Indexed as

Oxidative PhosphorylationCell DifferentiationCells, CulturedEmbryonic Stem CellsGlycolysisHumansInduced Pluripotent Stem CellsPluripotent Stem CellsReactive Oxygen SpeciesReactive Oxygen SpeciesDNA damage responsehistone acetylationhomeostatic balanceinduced pluripotent stem cellsoxidative phosphorylationreactive oxygen speciesROS

Identifiers

PMID29166598
PMCPMC5841608
OpenAlexW2769535462

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.