Evidence map›Paper›PMID 11245273›Full record

ReviewJournal of neuro-oncology

Nitric oxide and angiogenesis.

M Ziche, L Morbidelli

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neuro-oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 382 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Selective regulation of βMedical oncology (Northwood, London, England) · 2026
    Article
  5. Endothelial NMDA Receptor Involvement in Retinal Neurovascular Damage Following Prenatal Alcohol Exposure in a Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Exposure to Extreme Heat Increases Preterm Birth Risk: Hypothetical Pathophysiological Mechanisms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  13. Article
  14. Molecular Mediated Angiogenesis and Vasculogenesis Networks.International journal of molecular sciences · 2025
    Article
  15. Article
  16. Multifunctional Bionic Periosteum with Ion Sustained-Release for Bone Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  17. Review
  18. Article
  19. Article
  20. Article

54 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.

M ZicheInstitute of Pharmacological Sciences, University of Siena, Italy. ziche@unisi.it
L Morbidelli
University of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The steps required for new vessel growth are biologically complex and require coordinate regulation of contributing components, including modifications of cell--cell interactions, proliferation and migration of endothelial cells and matrix degradation. The observation that in vivo angiogenesis is accompanied by vasodilation, that many angiogenesis effectors possess vasodilating properties and that tumor vasculature is in a persistent state of vasodilation, support the existence of a molecular/biochemical link between vasodilation and angiogenesis. Several pieces of evidence converge in the indication of a role for nitric oxide (NO), the factor responsible for vasodilation, in physiological and pathological angiogenesis. Data originated in different labs indicate that NO can act both as an 'actor' of angiogenesis and as a 'director of angiogenesis', both functions being equally expressed during physiological and pathological processes. NO significantly contributes to the prosurvival/proangiogenic program of capillary endothelium by triggering and transducing cell growth and differentiation via endothelial-constitutive NO synthase (ec-NOS) activation, cyclic GMP (cGMP) elevation, mitogen activated kinase (MAPK) activation and fibroblast growth factor-2 (FGF-2) expression. Re-establishment of a balanced NO production in the central nervous system results in a reduction of cell damage during inflammatory and vascular diseases. Elevation of NOS activity in correlation with angiogenesis and tumor progression has been extensively reported in experimental and human tumors. In the brain, tumor expansion and edema formation are sensitive to NOS inhibition. On this basis, the nitric oxide pathway appears to be a promising target for consideration in pro- and anti-angiogenic therapeutic strategies. The use of NOS inhibitors seems appropriate to reduce edema, block angiogenesis and facilitate antitumor drug delivery.

Indexed as

Angiogenesis InhibitorsAnimalsEndothelium, VascularEnzyme InhibitorsHumansIsoenzymesMAP Kinase Signaling SystemMiceModels, BiologicalNeoplasm ProteinsNeoplastic Stem CellsNeovascularization, PathologicNeovascularization, PhysiologicNitric OxideNitric Oxide SynthaseRabbitsAngiogenesis InhibitorsEnzyme InhibitorsIsoenzymesNeoplasm ProteinsNitric OxideNitric Oxide Synthase

Identifiers

PMID11245273
OpenAlexW1525880745

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.