Evidence map›Paper›PMID 22841759›Full record

ReviewFree radical biology & medicine2012

Metabolic regulation of oxygen and redox homeostasis by p53: lessons from evolutionary biology?

Jie Zhuang, Wenzhe Ma, Cory U Lago, Paul M Hwang

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Cardiotoxicity of Cancer Treatments: Focus on Anthracycline Cardiomyopathy.Arteriosclerosis, thrombosis, and vascular biology · 2021
    Review
  6. Li-Fraumeni syndrome heterogeneity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
  7. Review
  8. p53 prevents doxorubicin cardiotoxicity independently of its prototypical tumor suppressor activities.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Twist and Turn-Topoisomerase Functions in Mitochondrial DNA Maintenance.International journal of molecular sciences · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. TP53 mutation, mitochondria and cancer.Current opinion in genetics & development · 2016
    Review
  16. Review
  17. Long story short: p53 mediates innate immunity.Biochimica et biophysica acta · 2016
    Review
  18. Review
  19. 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

4 authors at 2 institutions in 1 country.

Jie ZhuangCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Wenzhe Ma
Cory U Lago
Paul M Hwang
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Mitochondrial regulation in cardiovascular and cancer biologyZIAHL005101 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2009 to 2025
$19.1M
Redox homeostasis in cancer and cardiovascular diseasesZIAHL006051 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2010 to 2025
$12.8M
Genetic insights into atherosclerosis and other cardiovascular diseasesZIAHL006050 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2010 to 2020
$4.3M
Intramural NIH HHS ZIA HL005101Intramural NIH HHS ZIA HL006051
6 · The paper itself

Abstract

The genetic links between p53 and metabolic processes such as oxidative phosphorylation are being studied with increasing interest given that cellular metabolism seems to play an important role in tumorigenesis. This review focuses on how p53 regulation of various metabolic genes may influence redox homeostasis, as the genome is constantly susceptible to oxidative damage, a consequence of living in an aerobic environment. Because p53-like genetic sequences are also found in life forms that may not necessarily benefit from tumor suppression, an evolutionary introduction is given in an attempt to understand why p53 might regulate a basic cellular activity such as metabolism. The presented epidemiologic and experimental data suggest that one reason may be for the homeostatic regulation of oxygen, the essential substrate for reactive oxygen species generation.

Indexed as

Biological EvolutionHomeostasisAnimalsCell Transformation, NeoplasticGenomic InstabilityHumansMutationOxidation-ReductionOxidative StressOxygenTumor Suppressor Protein p53OxygenTumor Suppressor Protein p53

Identifiers

PMID22841759
PMCPMC3444283
OpenAlexW1981895506

What OpenQuestion holds

Textmetadata
LicenceTDM
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.