Evidence map›Paper›PMID 25695605›Full record

ArticleCell death & disease2015

Cellular oxidative stress response mediates radiosensitivity in Fus1-deficient mice.

E M Yazlovitskaya, P A Voziyan, T Manavalan, W G Yarbrough, A V Ivanova

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Altered Response to Total Body Irradiation of C57BL/6-Tg (CAG-EGFP) Mice.Dose-response : a publication of International Hormesis Society
    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

5 authors at 2 institutions in 1 country.

E M Yazlovitskaya1] Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA [2] Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, USA.
P A VoziyanDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
T ManavalanDepartment of Surgery, Division Otolaryngology, Yale School of Medicine, New Haven, CT, USA.
W G YarbroughDepartment of Surgery, Division Otolaryngology, Yale School of Medicine, New Haven, CT, USA.
A V IvanovaDepartment of Surgery, Division Otolaryngology, Yale School of Medicine, New Haven, CT, USA.
Yale University · USVanderbilt University · US

Funding

Glucose Modifications of Proteins in Diabetic NephropathyR01DK065138 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HUDSON, BILLY GERALD, VOZIYAN, PAUL A · 2003 to 2020
$6.3M
Role of the tumor suppressor Fus1 in asbestos-induced inflammatory cancersR21ES017496 · NIEHS · VANDERBILT UNIVERSITY · PI IVANOVA, ALLA V · 2010 to 2011
$425k
NIDDK NIH HHS R01 DK065138NIDDK NIH HHS R01DK65138NIEHS NIH HHS R21 ES017496NIEHS NIH HHS R21ES017496
6 · The paper itself

Abstract

Mechanism of radiosensitivity of normal tissues, a key factor in determining the toxic side effects of cancer radiotherapy, is not fully understood. We recently demonstrated that deficiency of mitochondrial tumor suppressor, Fus1, increases radiosensitivity at the organismal, tissue and cellular levels. Since Fus1-deficient mice and cells exhibit high levels of oxidative stress, we hypothesized that dysregulation of cellular antioxidant defenses may contribute to the increased radiosensitivity. To address this potential mechanism, we treated the Fus1 KO mice with an inhibitor of pathogenic oxidative reactions, pyridoxamine (PM). Treatment with PM ameliorated IR-induced damage to GI epithelium of Fus1 KO mice and significantly increased the survival of irradiated mice. In cultured Fus1 KO epithelial cells, IR-induced oxidative stress was enhanced because of inadequate cellular antioxidant defenses, such as low levels and/or activities of cytochrome C, Sod 2 and STAT3. This resulted in dysregulation of IR-induced DNA-damage response and DNA synthesis. Treatment of Fus1 KO cells with PM or Sod 2 mimetic Tempol normalized the oxidative stress response, thus compensating to a significant degree for inadequate antioxidant response. Our findings using Fus1 KO radiosensitive mice suggest that radiosensitivity is mediated via dysregulation of antioxidant response and defective redox homeostasis.

Indexed as

AnimalsCytochromes cDNA DamageFemaleMiceMice, KnockoutOxidative StressRadiation ToleranceSTAT3 Transcription FactorSuperoxide DismutaseSuperoxide Dismutase 2Tumor Suppressor ProteinsCytochromes cSTAT3 Transcription FactorSuperoxide DismutaseSuperoxide Dismutase 2Tumor Suppressor ProteinsTusc2 protein, mouse

Identifiers

PMID25695605
PMCPMC4669799
OpenAlexW2063761125

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.