Evidence map›Paper›PMID 22519544›Full record

ArticleBritish journal of pharmacology2012

Involvement of redox-signalling in endogenous hydrogen sulfide production.

Ferenc Gallyas

Abstract readComment
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Ferenc GallyasDepartment of Biochemistry and Medical Chemistry, University of Pecs Medical School, Pecs, Hungary Nuclear-Mitochondrial Interactions Research Group, Hungarian Academy of Sciences, Budapest, Hungary. ferenc.gallyas@aok.pte.hu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledRecently, cystathionine-γ-lyase (CSE) was found to provide the major physiological pathway for H(2) S, the third member of the gasotransmitter family. In various pathophysiological conditions, H(2) S exerted protective effects based on its antioxidant, anti-inflammatory, anti-hypertensive and other regulatory functions. Interestingly, CSE expression had been only poorly studied and only in relation with inflammatory processes. Therefore, the study by Hassan et al. in this issue of the BJP, provides a considerable advance by furnishing direct experimental evidence for the involvement of redox signalling in the regulation of CSE gene expression. They found that PDGF up-regulated CSE expression and activity that was abolished by antioxidants and by deletion of the transcription factor nuclear erythroid-2-related factor-2 (Nrf2). Furthermore, PDGF induced Nrf2 binding to its consensus sequence that was again reversed by antioxidants. As Nrf2 also governs CO biosynthesis, and PDGF inversely affects H(2) S and NO production, these data could indicate a concerted regulation of the three gasotransmitters by redox signalling. LINKED ARTICLE: This article is a commentary on Hassan et al., pp. 2231-2242 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2012.01949.x.

Indexed as

AnimalsBecaplerminCystathionine gamma-LyaseGene Expression Regulation, EnzymologicMesangial CellsProto-Oncogene Proteins c-sisBecaplerminCystathionine gamma-LyaseProto-Oncogene Proteins c-sis

Identifiers

PMID22519544
PMCPMC3448889

What OpenQuestion holds

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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.