Evidence map›Paper›PMID 28956814›Full record

ReviewAntioxidants (Basel, Switzerland)2017

Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses.

Chontida Yarana, Daret K St Clair

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07651787 (Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment), which is not on this map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.7field-weighted citation impact, top 16% 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.

NCT07651787 narecruitingnot on this mapstarted 2025, after this paper: background citation

Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment

TypeinterventionalSponsorUniversity of OklahomaRan2025 to 2026Enrolled40ConditionsMild Cognitive Impairment (MCI), Amyloid PathologyArmsActive Vielight Neuro RX-Duo device -Active transcranial photobiomodulation, Sham Vielight Neuro RX-Duo device -Sham transcranial photobiomodulation
3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Vincamine Mitigates Methotrexate-Induced Liver Fibrosis Model.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Exosome Mediated Cell-Cell Crosstalk in Tissue Injury and Repair.Results and problems in cell differentiation · 2024
    Review
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

2 authors at 1 institution in 2 countries.

Chontida YaranaDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY 40536, USA. cya224@g.uky.edu.
Daret K St ClairDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY 40536, USA. dstcl00@uky.edu.
University of Kentucky · US

Funding

MbSOD in chemotherapeutic-Induced Cardiac InjuryR01CA139843 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 2008 to 2012
$1.3M
NCI NIH HHS R01 CA139843
6 · The paper itself

Abstract

The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating health impacts. Approximately half of the drugs approved by the Food and Drug Administration for cancer treatment are associated with the generation of reactive oxygen species, and Doxorubicin (Dox) is one of them. Dox undergoes redox cycling by involving its quinone structure in the production of superoxide free radicals, which are thought to be instrumental to the role it plays in cardiomyopathy. Dox-induced protein oxidation changes protein function, translocation, and aggregation that are toxic to cells. To maintain cellular homeostasis, oxidized proteins can be degraded intracellularly by ubiquitin-proteasome pathway or by autophagy, depending on the redox status of the cell. Alternatively, the cell can remove oxidized proteins by releasing extracellular vesicles (EVs), which can be transferred to neighboring or distant cells, thereby instigating an intercellular oxidative stress response. In this article, we discuss the role of EVs in oxidative stress response, the potential of EVs as sensitive biomarkers of oxidative stress, and the role of superoxide dismutase in attenuating EV-associated oxidative stress response resulting from chemotherapy.

Indexed as

chemotherapyextracellular vesiclesoxidative stresssuperoxide dismutase

Identifiers

PMID28956814
PMCPMC5745485
OpenAlexW2760707643

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.