Evidence map›Paper›PMID 27478531›Full record

ReviewOxidative medicine and cellular longevity2016

Role of ROS and RNS Sources in Physiological and Pathological Conditions.

Sergio Di Meo, Tanea T Reed, Paola Venditti, Victor Manuel Victor

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 720 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
720citing papers in PubMed, 1 pooled it
45.3field-weighted citation impact, top 1% 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

720 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,565 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Iron Overload: Pathophysiology, Diagnosis and Monitoring.International journal of laboratory hematology · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. The Oxidative Stress: Origin and Role in Aging and Diseases.Antioxidants (Basel, Switzerland) · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

660 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Sergio Di MeoDipartimento di Biologia, Università di Napoli "Federico II", 80126 Napoli, Italy.ORCID 0000-0002-4602-9146
Tanea T ReedDepartment of Chemistry, Eastern Kentucky University, Richmond, KY 40475, USA.ORCID 0000-0003-2642-3100
Paola VendittiDipartimento di Biologia, Università di Napoli "Federico II", 80126 Napoli, Italy.ORCID 0000-0003-0522-1788
Victor Manuel VictorService of Endocrinology, University Hospital Dr. Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), 46010 Valencia, Spain.
University of Naples Federico II · ITEastern Kentucky University · USFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is significant evidence that, in living systems, free radicals and other reactive oxygen and nitrogen species play a double role, because they can cause oxidative damage and tissue dysfunction and serve as molecular signals activating stress responses that are beneficial to the organism. Mitochondria have been thought to both play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction through several mechanisms, including stimulation of opening of permeability transition pores. Until recently, the functional significance of ROS sources different from mitochondria has received lesser attention. However, the most recent data, besides confirming the mitochondrial role in tissue oxidative stress and protection, show interplay between mitochondria and other ROS cellular sources, so that activation of one can lead to activation of other sources. Thus, it is currently accepted that in various conditions all cellular sources of ROS provide significant contribution to processes that oxidatively damage tissues and assure their survival, through mechanisms such as autophagy and apoptosis.

Indexed as

AnimalsApoptosisCytosolEndoplasmic ReticulumHumansLysosomesMitochondriaMultienzyme ComplexesNADH, NADPH OxidoreductasesOxidative StressPeroxisomesReactive Nitrogen SpeciesReactive Oxygen SpeciesMultienzyme ComplexesNADH, NADPH OxidoreductasesNADH oxidaseReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID27478531
PMCPMC4960346
OpenAlexW2468879160

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.