Evidence map›Paper›PMID 26064427›Full record

ReviewOxidative medicine and cellular longevity2015

Arginase as a Critical Prooxidant Mediator in the Binomial Endothelial Dysfunction-Atherosclerosis.

Luiza A Rabelo, Fernanda O Ferreira, Valéria Nunes-Souza, Lucas José Sá da Fonseca, Marília O F Goulart

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Understanding the links between cardiovascular disease and Parkinson's disease.Movement disorders : official journal of the Movement Disorder Society · 2020
    Review
  10. Frontiers in physiology · 2020
    Article
  11. Cross-Talk between Oxidative Stress and Inflammation in Preeclampsia.Oxidative medicine and cellular longevity · 2019
    Review
  12. Review
  13. Chitosan treatment abrogates hypercholesterolemia-induced erythrocyte's arginase activation.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2017
    Article
  14. 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

5 authors at 2 institutions in 2 countries.

Luiza A RabeloLaboratório de Reatividade Cardiovascular, Setor de Fisiologia e Farmacologia, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil ; Instituto Nacional de Ciência e Tecnologia em NanoBiofarmacêutica (N-BIOFAR), Avenida Antônio Carlos s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil ; Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
Fernanda O FerreiraLaboratório de Reatividade Cardiovascular, Setor de Fisiologia e Farmacologia, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil ; Instituto Nacional de Ciência e Tecnologia em NanoBiofarmacêutica (N-BIOFAR), Avenida Antônio Carlos s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil.
Valéria Nunes-SouzaLaboratório de Reatividade Cardiovascular, Setor de Fisiologia e Farmacologia, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil ; Instituto Nacional de Ciência e Tecnologia em NanoBiofarmacêutica (N-BIOFAR), Avenida Antônio Carlos s/n, Pampulha, 31270-901 Belo Horizonte, MG, Brazil ; Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
Lucas José Sá da FonsecaLaboratório de Reatividade Cardiovascular, Setor de Fisiologia e Farmacologia, Instituto de Ciências Biológicas e da Saúde (ICBS), Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil.
Marília O F GoulartInstituto de Química e Biotecnologia, Universidade Federal de Alagoas (UFAL), Avenida Lourival Melo Mota s/n, Cidade Universitária, 57072-900 Maceió, AL, Brazil.
Universidade Federal de Alagoas · BRMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arginase is a metalloenzyme which hydrolyzes L-arginine to L-ornithine and urea. Since its discovery, in the early 1900s, this enzyme has gained increasing attention, as literature reports have progressively pointed to its critical participation in regulating nitric oxide bioavailability. Indeed, accumulating evidence in the following years would picture arginase as a key player in vascular health. Recent studies have highlighted the arginase regulatory role in the progression of atherosclerosis, the latter an essentially prooxidant state. Apart from the fact that arginase has been proven to impair different metabolic pathways, and also as a consequence of this, the repercussions of the actions of such enzyme go further than first thought. In fact, such metalloenzyme exhibits direct implications in multiple cardiometabolic diseases, among which are hypertension, type 2 diabetes, and hypercholesterolemia. Considering the epidemiological repercussions of these clinical conditions, arginase is currently seen under the spotlights of the search for developing specific inhibitors, in order to mitigate its deleterious effects. That said, the present review focuses on the role of arginase in endothelial function and its participation in the establishment of atherosclerotic lesions, discussing the main regulatory mechanisms of the enzyme, also highlighting the potential development of pharmacological strategies in related cardiovascular diseases.

Indexed as

AnimalsArginaseAtherosclerosisEndothelium, VascularHumansNitric OxideNitric Oxide Synthase Type IIISignal TransductionArginaseNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID26064427
PMCPMC4434223
OpenAlexW1580652849

What OpenQuestion holds

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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.