Evidence map›Paper›PMID 31067778›Full record

ReviewInternational journal of molecular sciences2019

Mechanisms of the Metabolic Shift during Somatic Cell Reprogramming.

Ken Nishimura, Aya Fukuda, Koji Hisatake

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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  5. Review
  6. The Mammalian Oocyte: A Central Hub for Cellular Reprogramming and Stemness.Stem cells and cloning : advances and applications · 2025
    Review
  7. BRG1 improves reprogramming efficiency by enhancing glycolytic metabolism.Cellular and molecular life sciences : CMLS · 2024
    Article
  8. NFκB and JNK pathways mediate metabolic adaptation upon ESCRT-I deficiency.Cellular and molecular life sciences : CMLS · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. "Time Is out of Joint" in Pluripotent Stem Cells: How and Why.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Review
  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

3 authors.

Ken NishimuraLaboratory of Gene Regulation, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Japan. ken-nishimura@md.tsukuba.ac.jp.
Aya FukudaLaboratory of Gene Regulation, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Japan. fukudaa@md.tsukuba.ac.jp.
Koji HisatakeLaboratory of Gene Regulation, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Japan. kojihisa@md.tsukuba.ac.jp.ORCID 0000-0002-5795-3115

Funding

Japan Society for the Promotion of Science JP16K08610Japan Society for the Promotion of Science JP25460354Japan Society for the Promotion of Science JP26870074
6 · The paper itself

Abstract

Pluripotent stem cells (PSCs), including embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), hold a huge promise for regenerative medicine, drug development, and disease modeling. PSCs have unique metabolic features that are akin to those of cancer cells, in which glycolysis predominates to produce energy as well as building blocks for cellular components. Recent studies indicate that the unique metabolism in PSCs is not a mere consequence of their preference for a low oxygen environment, but is an active process for maintaining self-renewal and pluripotency, possibly in preparation for rapid response to the metabolic demands of differentiation. Understanding the regulatory mechanisms of this unique metabolism in PSCs is essential for proper derivation, generation, and maintenance of PSCs. In this review, we discuss the metabolic features of PSCs and describe the current understanding of the mechanisms of the metabolic shift during reprogramming from somatic cells to iPSCs, in which the metabolism switches from oxidative phosphorylation (OxPhos) to glycolysis.

Indexed as

Cellular ReprogrammingEnergy MetabolismAnimalsHumansMitochondriaPluripotent Stem CellsESChypoxiaiPSCmetabolismmitochondrionOxPhos: glycolysisPSCsomatic cell reprogramming

Identifiers

PMID31067778
PMCPMC6539623

What OpenQuestion holds

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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.