Evidence map›Paper›PMID 22719764›Full record

ArticleInternational journal of cell biology2012

Nitric oxide inactivation mechanisms in the brain: role in bioenergetics and neurodegeneration.

Ricardo M Santos, Cátia F Lourenço, Ana Ledo, Rui M Barbosa, João Laranjinha

Abstract read
In one paragraph

Article in International journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

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  11. Gasotransmitter Heterocellular Signaling.Antioxidants & redox signaling · 2017
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  16. Effects of nitric oxide on magnocellular neurons of the supraoptic nucleus involve multiple mechanisms.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
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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

5 authors.

Ricardo M SantosFaculty of Pharmacy and Center for Neurosciences and Cell Biology, University of Coimbra, Health Sciences Campus, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal.
Cátia F Lourenço
Ana Ledo
Rui M Barbosa
João Laranjinha

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the last decades nitric oxide ((•)NO) has emerged as a critical physiological signaling molecule in mammalian tissues, notably in the brain. (•)NO may modify the activity of regulatory proteins via direct reaction with the heme moiety, or indirectly, via S-nitrosylation of thiol groups or nitration of tyrosine residues. However, a conceptual understanding of how (•)NO bioactivity is carried out in biological systems is hampered by the lack of knowledge on its dynamics in vivo. Key questions still lacking concrete and definitive answers include those related with quantitative issues of its concentration dynamics and diffusion, summarized in the how much, how long, and how far trilogy. For instance, a major problem is the lack of knowledge of what constitutes a physiological (•)NO concentration and what constitutes a pathological one and how is (•)NO concentration regulated. The ambient (•)NO concentration reflects the balance between the rate of synthesis and the rate of breakdown. Much has been learnt about the mechanism of (•)NO synthesis, but the inactivation pathways of (•)NO has been almost completely ignored. We have recently addressed these issues in vivo on basis of microelectrode technology that allows a fine-tuned spatial and temporal measurement (•)NO concentration dynamics in the brain.

Identifiers

PMID22719764
PMCPMC3376480

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Registered trials

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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.