Evidence map›Paper›PMID 31993367›Full record

ReviewFrontiers in oncology2019

Inhibition of Dimethylarginine Dimethylaminohydrolase (DDAH) Enzymes as an Emerging Therapeutic Strategy to Target Angiogenesis and Vasculogenic Mimicry in Cancer.

Julie-Ann Hulin, Ekaterina A Gubareva, Natalia Jarzebska, Roman N Rodionov, Arduino A Mangoni, Sara Tommasi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2019. 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
3.2field-weighted citation impact, top 8% 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, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Emerging Role of the DDAH Proteins in Psychiatric Disorders.Biological psychiatry global open science · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Mass Spectrometry Analysis of Shark Skin Proteins.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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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

6 authors at 3 institutions in 3 countries.

Julie-Ann HulinClinical Pharmacology, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Ekaterina A GubarevaN.N. Petrov National Medical Research Center of Oncology, Saint Petersburg, Russia.
Natalia JarzebskaDivision of Angiology, Department of Internal Medicine III, University Center for Vascular Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Roman N RodionovDivision of Angiology, Department of Internal Medicine III, University Center for Vascular Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Arduino A MangoniClinical Pharmacology, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Sara TommasiClinical Pharmacology, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Flinders University · AUUniversity Hospital Carl Gustav Carus · DEInstitute of Oncology NN Petrov · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small free radical gas nitric oxide (NO) plays a key role in various physiological and pathological processes through enhancement of endothelial cell survival and proliferation. In particular, NO has emerged as a molecule of interest in carcinogenesis and tumor progression due to its crucial role in various cancer-related events including cell invasion, metastasis, and angiogenesis. The dimethylarginine dimethylaminohydrolase (DDAH) family of enzymes metabolize the endogenous nitric oxide synthase (NOS) inhibitors, asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA), and are thus key for maintaining homeostatic control of NO. Dysregulation of the DDAH/ADMA/NO pathway resulting in increased local NO availability often promotes tumor growth, angiogenesis, and vasculogenic mimicry. Recent literature has demonstrated increased DDAH expression in tumors of different origins and has also suggested a potential ADMA-independent role for DDAH enzymes in addition to their well-studied ADMA-mediated influence on NO. Inhibition of DDAH expression and/or activity in cell culture models and

Indexed as

ADMAangiogenesiscancerDDAHnitric oxidevasculogenic mimicry

Identifiers

PMID31993367
PMCPMC6962312
OpenAlexW3000138326

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.