Evidence map›Paper›PMID 18437360›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2008

Arginase and pulmonary diseases.

Harm Maarsingh, Tonio Pera, Herman Meurs

Open access · hybridAbstract readReview
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
6.6field-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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Regulatory haplotypes in ARG1 are associated with altered bronchodilator response.American journal of respiratory and critical care medicine · 2011
    Trial
  4. Article
  5. Article
  6. Article
  7. Characteristics ofFrontiers in immunology · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Therapeutic targeting of argininosuccinate synthase 1 (ASS1)-deficient pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  18. Article
  19. Article
  20. Article

3 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

3 authors at 1 institution in 1 country.

Harm MaarsinghDepartment of Molecular Pharmacology, University Centre for Pharmacy, University of Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands. h.maarsingh@rug.nl
Tonio Pera
Herman Meurs
University of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have indicated that arginase, which converts L-arginine into L-ornithine and urea, may play an important role in the pathogenesis of various pulmonary disorders. In asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis, increased arginase activity in the airways may contribute to obstruction and hyperresponsiveness of the airways by inducing a reduction in the production of bronchodilatory nitric oxide (NO) that results from its competition with constitutive (cNOS) and inducible (iNOS) NO synthases for their common substrate. In addition, reduced L-arginine availability to iNOS induced by arginase may result in the synthesis of both NO and the superoxide anion by this enzyme, thereby enhancing the production of peroxynitrite, which has procontractile and pro-inflammatory actions. Increased synthesis of L-ornithine by arginase may also contribute to airway remodelling in these diseases. L-Ornithine is a precursor of polyamines and L-proline, and these metabolic products may promote cell proliferation and collagen production, respectively. Increased arginase activity may also be involved in other fibrotic disorders of the lung, including idiopathic pulmonary fibrosis. Finally, through its action of inducing reduced levels of vasodilating NO, increased arginase activity has been associated with primary and secondary forms of pulmonary hypertension. Drugs targeting the arginase pathway could have therapeutic potential in these diseases.

Indexed as

AnimalsArginaseArginineAsthmaCystic FibrosisDisease Models, AnimalHumansHypertension, PulmonaryLungLung DiseasesNitric OxideNitric Oxide SynthaseOrnithinePulmonary Disease, Chronic ObstructivePulmonary FibrosisUreaArginaseArginineNitric OxideNitric Oxide SynthaseOrnithineUrea

Identifiers

PMID18437360
PMCPMC2493601
OpenAlexW2118154607

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.