Evidence map›Paper›PMID 37534225›Full record

ReviewEXCLI journal2023

The bridge between cell survival and cell death: reactive oxygen species-mediated cellular stress.

Nese Vardar Acar, Riza Köksal Özgül

Open access · greenAbstract readReview
In one paragraph

Review in EXCLI journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Food science & nutrition · 2025
    Review
  6. Nanotherapies Based on ROS Regulation in Oral Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. 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 1 country.

Nese Vardar AcarDepartment of Pediatric Metabolism, Institute of Child Health, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Riza Köksal ÖzgülDepartment of Pediatric Metabolism, Institute of Child Health, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Hacettepe University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a requirement of aerobic metabolism, regulation of redox homeostasis is indispensable for the continuity of living homeostasis and life. Since the stability of the redox state is necessary for the maintenance of the biological functions of the cells, the balance between the pro-oxidants, especially ROS and the antioxidant capacity is kept in balance in the cells through antioxidant defense systems. The pleiotropic transcription factor, Nrf2, is the master regulator of the antioxidant defense system. Disruption of redox homeostasis leads to oxidative and reductive stress, bringing about multiple pathophysiological conditions. Oxidative stress characterized by high ROS levels causes oxidative damage to biomolecules and cell death, while reductive stress characterized by low ROS levels disrupt physiological cell functions. The fact that ROS, which were initially attributed as harmful products of aerobic metabolism, at the same time function as signal molecules at non-toxic levels and play a role in the adaptive response called mithormesis points out that ROS have a dose-dependent effect on cell fate determination. See also Figure 1(Fig. 1).

Indexed as

antioxidant defense systemscell death pathwaysmitohormesisNrf2oxidative and reductive stressredox homeostasis

Identifiers

PMID37534225
PMCPMC10390897
OpenAlexW4385513914

What Socratic 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 Socratic graph.