Evidence map›Paper›PMID 26877834›Full record

ReviewToxicological research2015

Mitochondria in Cancer Energy Metabolism: Culprits or Bystanders?

Aekyong Kim

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicological research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Cancer as a Metabolic Disorder.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Analysis of Hematopoietic Stem Progenitor Cell Metabolism.Journal of visualized experiments : JoVE · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. In colonic ρOncoscience · 2017
    Article
  18. Article
  19. Reduced mitochondrial activity in colonocytes facilitates AMPKα2-dependent inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  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

1 author at 1 institution in 1 country.

Aekyong KimSchool of Pharmacy, Catholic University of Daegu, Gyeongbuk, Korea.
Catholic University of Daegu · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is a disease characterized by uncontrolled growth. Metabolic demands to sustain rapid proliferation must be compelling since aerobic glycolysis is the first as well as the most commonly shared characteristic of cancer. During the last decade, the significance of metabolic reprogramming of cancer has been at the center of attention. Nonetheless, despite all the knowledge gained on cancer biology, the field is not able to reach agreement on the issue of mitochondria: Are damaged mitochondria the cause for aerobic glycolysis in cancer? Warburg proposed the damaged mitochondria theory over 80 years ago; the field has been testing the theory equally long. In this review, we will discuss alterations in metabolic fluxes of cancer cells, and provide an opinion on the damaged mitochondria theory.

Indexed as

Aerobic glycolysisAnaplerosisCancerCataplerosisGlutaminolysisMetabolismMitochondria

Identifiers

PMID26877834
PMCPMC4751441
OpenAlexW2336469753

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.