Evidence map›Paper›PMID 22198555›Full record

ReviewCellular and molecular neurobiology2012

Current therapeutic strategies to mitigate the eNOS dysfunction in ischaemic stroke.

Kirtiman Srivastava, Philip M W Bath, Ulvi Bayraktutan

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Regulatory effects of trimetazidine in cardiac ischemia/reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  7. Article
  8. Article
  9. Photobiomodulation and nitric oxide signaling.Nitric oxide : biology and chemistry · 2023
    Review
  10. Near-infrared II photobiomodulation augments nitric oxide bioavailability via phosphorylation of endothelial nitric oxide synthase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  11. Mastoparan M extracted fromIranian journal of basic medical sciences · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Kirtiman SrivastavaDivision of Stroke, Clinical Sciences Building, Nottingham City Hospital Campus, The University of Nottingham, Nottingham, UK. msxks1@nottingham.ac.uk
Philip M W Bath
Ulvi Bayraktutan
Nottingham City Hospital · GB

Funding

Medical Research Council G0501797
6 · The paper itself

Abstract

Impairment of endothelial nitric oxide synthase (eNOS) activity is implicated in the pathogenesis of endothelial dysfunction in many diseases including ischaemic stroke. The modulation of eNOS during and/or following ischaemic injury often represents a futile compensatory mechanism due to a significant decrease in nitric oxide (NO) bioavailability coupled with dramatic increases in the levels of reactive oxygen species that further neutralise NO. However, applications of a number of therapeutic agents alone or in combination have been shown to augment eNOS activity under a variety of pathological conditions by potentiating the expression and/or activity of Akt/eNOS/NO pathway components. The list of these therapeutic agents include NO donors, statins, angiotensin-converting enzyme inhibitors, calcium channel blockers, phosphodiesterase-3 inhibitors, aspirin, dipyridamole and ellagic acid. While most of these compounds exhibit anti-platelet properties and are able to up-regulate eNOS expression in endothelial cells and platelets, others suppress eNOS uncoupling and tetrahydrobiopterin (an eNOS stabiliser) oxidation. As the number of therapeutic molecules that modulate the expression and activity of eNOS increases, further detailed research is required to reveal their mode of action in preventing and/or reversing the endothelial dysfunction.

Indexed as

AnimalsBrain IschemiaHumansNeural PathwaysNitric Oxide Synthase Type IIIStrokeUp-RegulationNitric Oxide Synthase Type III

Identifiers

PMID22198555
PMCPMC11498629
OpenAlexW2063449407

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.