Evidence map›Paper›PMID 16771683›Full record

ReviewAntioxidants & redox signaling

Regulation of inducible nitric oxide synthase gene in glial cells.

Ramendra N Saha, Kalipada Pahan

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

179 citing papers in PubMed, 348 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Benzoate Drugs for Traumatic Brain Injury.Journal of clinical & experimental immunology · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Redox modulation of the complement cascade contributes to synapse loss in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

119 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

2 authors at 1 institution in 1 country.

Ramendra N SahaDepartment of Oral Biology, Section of Neuroscience, University of Nebraska Medical Center, Lincoln, 68583, USA.
Kalipada Pahan
University of Nebraska–Lincoln · US

Funding

ACTIVATION OF NF-KB IN GLIAL CELLS AND CNS OF EAER01NS039940 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PAHAN, KALIPADA · 2001 to 2009
$2.7M
Statin and Phenylacetate in MPTP Mouse ModelR21NS048923 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PAHAN, KALIPADA · 2006 to 2007
$327k
NINDS NIH HHS NS39940NINDS NIH HHS NS48923NINDS NIH HHS R01 NS039940NINDS NIH HHS R21 NS048923
6 · The paper itself

Abstract

Elevated levels of NO produced within the central nervous system (CNS) are associated with the pathogenesis of neuroinflammatory and neurodegenerative human diseases such as multiple sclerosis, HIV dementia, brain ischemia, trauma, Parkinson's disease, and Alzheimer's disease. Resident glial cells in the CNS (astroglia and microglia) express inducible nitric oxide synthase (iNOS) and produce high levels of NO in response to a wide variety of proinflammatory and degenerative stimuli. Although pathways resulting in the expression of iNOS may vary in two different glial cells of different species, the intracellular signaling events required for the expression of iNOS in these cells are slowly becoming clear. Various signaling cascades converge to activate several transcription factors that control the transcription of iNOS in glial cells. The present review summarizes different results and discusses current understandings about signaling mechanisms for the induction of iNOS expression in activated glial cells. A complete understanding of the regulation of iNOS expression in glial cells is expected to identify novel targets for therapeutic intervention in NO-mediated neurological disorders.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsBacteriaCyclic AMPCytokinesHumansMevalonic AcidMitogen-Activated Protein KinasesNeurogliaNitric Oxide Synthase Type IIPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesProtein-Tyrosine KinasesReactive Oxygen SpeciesSuppressor of Cytokine Signaling ProteinsTranscription FactorsCyclic AMPCytokinesMevalonic AcidMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesProtein-Tyrosine KinasesReactive Oxygen SpeciesSuppressor of Cytokine Signaling ProteinsTranscription Factors

Identifiers

PMID16771683
PMCPMC1963415
OpenAlexW2037043234

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.