Evidence map›Paper›PMID 19745170›Full record

ReviewCirculation research2009

Cardiovascular consequences when nitric oxide and lipid signaling converge.

Volker Rudolph, Bruce A Freeman

Abstract readReview
In one paragraph

Review in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Circadian rhythm and atherosclerosis (Review).Experimental and therapeutic medicine · 2020
    Review
  5. Review
  6. Ischemia/Reperfusion.Comprehensive Physiology · 2016
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Relationship between deep venous thrombosis and inflammatory cytokines in postoperative patients with malignant abdominal tumors.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
  12. Organic nitrates: past, present and future.Molecules (Basel, Switzerland) · 2014
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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 2 countries.

Volker RudolphDepartment of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Bruce A Freeman
Universität Hamburg · DE

Funding

Redox-Derived Pulmonary Anti-Inflammatory MediatorsR01HL064937 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2000 to 2015
$5.6M
NITRIC OXIDE REGULATION OF VASCULAR OXIDANT INJURYR01HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 1998 to 2007
$3.3M
NHLBI NIH HHS R01 HL058115NHLBI NIH HHS R01 HL064937NHLBI NIH HHS R01 HL58115NHLBI NIH HHS R01 HL64937
6 · The paper itself

Abstract

The identification of nitric oxide ((*)NO) as an endogenously produced free radical mediator of endothelial-dependent relaxation and host defense has fundamentally changed concepts of cell signal transduction. Ligand-receptor oriented paradigms of cell signaling were originally centered on the concept of a high affinity and specific interaction between a ligand and its receptor, resulting in the activation of secondary signaling events such as gene expression or modulation of catalytic protein function. While (*)NO ligation of the heme iron of soluble guanylate cyclase is consistent with this perspective, the readily diffusible and broadly reactive (*)NO is increasingly appreciated to react with a vast array of target molecules that mediate paracrine vasodilator actions, inhibition of thrombosis and neointimal proliferation, and both pro- and antiinflammatory signaling reactions that are not affected by inhibitors of soluble guanylate cyclase. There is an expanding array of functionally significant "off target" collateral reactions mediated by (*)NO that are guanylate cyclase-independent and rather are dictated by anatomic distribution and the formation of secondary (*)NO-derived species. These reactions are a critical element of redox-regulated signaling and are addressed herein in the context of the oxidation of unsaturated fatty acids to vascular and inflammatory signaling mediators. Because of their abundance and the intrinsic reactivity of unsaturated lipid intermediates and eicosanoid metabolism enzymes with (*)NO and other oxides of nitrogen, lipid signaling mechanisms are a significant target for regulation by (*)NO in the vascular compartment. This convergence of (*)NO and lipid signaling pathways thus adds another level of regulation to physiological responses such as vasodilation, thrombosis, and inflammation. Herein, interactions between (*)NO and lipid signaling events are placed in the context of cardiovascular regulation.

Indexed as

Paracrine CommunicationSignal TransductionCell ProliferationEicosanoidsFatty AcidsGuanylate CyclaseHemeInflammationInflammation MediatorsIronNitric OxideOxidation-ReductionThrombosisTunica IntimaVasodilationEicosanoidsFatty AcidsGuanylate CyclaseHemeInflammation MediatorsIronNitric Oxide

Identifiers

PMID19745170
PMCPMC2773707
OpenAlexW2097996389

What OpenQuestion holds

Textmetadata
LicenceTDM
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.