Evidence map›Paper›PMID 31500396›Full record

ReviewCells2019

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer.

Hung-Chi Yang, Yi-Hsuan Wu, Wei-Chen Yen, Hui-Ya Liu, Tsong-Long Hwang, Arnold Stern, Daniel Tsun-Yee Chiu

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 1 pooled it
44.5field-weighted citation impact, top 1% 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

146 citing papers in PubMed, 1 synthesis or guideline pooled it, 251 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Implications of host sex on liver metabolism duringFrontiers in cellular and infection microbiology · 2026
    Review
  10. Article
  11. Review
  12. No G6PD A- (G202A) variant detected amongMalariaWorld journal · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Targeting G6PD with Benzimidazole and Thiazole Derivatives SuppressesInternational journal of molecular sciences · 2025
    Article
  18. Article
  19. Article
  20. Review

86 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Hung-Chi YangDepartment of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu, Taiwan. hcyang@mail.ypu.edu.tw.
Yi-Hsuan WuResearch Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan. yhwu03@mail.cgust.edu.tw.
Wei-Chen YenGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. d56610@yahoo.com.tw.
Hui-Ya LiuDepartment of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. liuhy@mail.cgu.edu.tw.
Tsong-Long HwangResearch Center for Food and Cosmetic Safety, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan. htl@mail.cgu.edu.tw.
Arnold SternNew York University School of Medicine, New York, NY, USA. stern@nyulangone.org.
Daniel Tsun-Yee ChiuDepartment of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. dtychiu@mail.cgu.edu.tw.
Chang Gung University · TWChang Gung University of Science and Technology · TWMing Chi University of Technology · TWNew York University · USYuanpei University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance of redox homeostasis and reductive biosynthesis in cells. NADPH also plays key roles in cellular processes mediated by redox signaling. Insufficient G6PD activity predisposes cells to growth retardation and demise. Severely lacking G6PD impairs embryonic development and delays organismal growth. Altered G6PD activity is associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, as well as diabetes and hypertension. Aberrant activation of G6PD leads to enhanced cell proliferation and adaptation in many types of cancers. The present review aims to update the existing knowledge concerning G6PD and emphasizes how G6PD modulates redox signaling and affects cell survival and demise, particularly in diseases such as cancer. Exploiting G6PD as a potential drug target against cancer is also discussed.

Indexed as

Cell CycleCell DeathCell ProliferationCell SurvivalGlucosephosphate DehydrogenaseGlucosephosphate Dehydrogenase DeficiencyHomeostasisHumansNADPNeoplasmsOxidation-ReductionPentose Phosphate PathwayReactive Oxygen SpeciesSignal TransductionGlucosephosphate DehydrogenaseNADPReactive Oxygen Speciescancercell deathcell growthG6PDredox signaling

Identifiers

PMID31500396
PMCPMC6770671
OpenAlexW2971580085

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.