Evidence map›Paper›PMID 25263488›Full record

ReviewCellular & molecular immunology2015

NADPH oxidases: an overview from structure to innate immunity-associated pathologies.

Arvind Panday, Malaya K Sahoo, Diana Osorio, Sanjay Batra

Open access · bronzeAbstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 510 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
510citing papers in PubMed, 1 pooled it
15.7field-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

510 citing papers in PubMed, 1 synthesis or guideline pooled it, 908 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

450 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 1 country.

Arvind PandayDepartment of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA.
Malaya K SahooDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Diana OsorioDepartment of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA.
Sanjay Batra1] Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA [2] Department of Environmental Toxicology, Southern University and A&M College, Baton Rouge, Louisiana 70813.
Louisiana State University · USSouthern University and Agricultural and Mechanical College · USStanford University · US

Funding

NOD-Like Receptor Signaling is Critical to Secondhand Smoke-Induced Immunity andR15ES023151 · NIEHS · SOUTHERN UNIV A&M COL BATON ROUGE · PI BATRA, SANJAY · 2013 to 2016
$369k
NIEHS NIH HHS R15-1R15ES023151-01NIEHS NIH HHS R15 ES023151
6 · The paper itself

Abstract

Oxygen-derived free radicals, collectively termed reactive oxygen species (ROS), play important roles in immunity, cell growth, and cell signaling. In excess, however, ROS are lethal to cells, and the overproduction of these molecules leads to a myriad of devastating diseases. The key producers of ROS in many cells are the NOX family of NADPH oxidases, of which there are seven members, with various tissue distributions and activation mechanisms. NADPH oxidase is a multisubunit enzyme comprising membrane and cytosolic components, which actively communicate during the host responses to a wide variety of stimuli, including viral and bacterial infections. This enzymatic complex has been implicated in many functions ranging from host defense to cellular signaling and the regulation of gene expression. NOX deficiency might lead to immunosuppression, while the intracellular accumulation of ROS results in the inhibition of viral propagation and apoptosis. However, excess ROS production causes cellular stress, leading to various lethal diseases, including autoimmune diseases and cancer. During the later stages of injury, NOX promotes tissue repair through the induction of angiogenesis and cell proliferation. Therefore, a complete understanding of the function of NOX is important to direct the role of this enzyme towards host defense and tissue repair or increase resistance to stress in a timely and disease-specific manner.

Indexed as

AnimalsDNA DamageHumansImmune System DiseasesImmunity, InnateInfectionsMolecular ConformationNADH, NADPH OxidoreductasesNeovascularization, PhysiologicReactive Oxygen SpeciesStructure-Activity RelationshipWound HealingNADH, NADPH OxidoreductasesReactive Oxygen Species

Identifiers

PMID25263488
PMCPMC4654378
OpenAlexW2167872299

What OpenQuestion holds

Textmetadata
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.