Evidence map›Paper›PMID 19641690›Full record

ArticleExperimental and clinical cardiology2004

The role of free radicals in endogenous adaptation and intracellular signals.

E Röth, L Hejjel, Mt Jaberansari, G Jancso

Open access · greenAbstract read
In one paragraph

Article in Experimental and clinical cardiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact, top 83% 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

7 citing papers in PubMed, 22 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

E RöthDepartment of Experimental Surgery, University of Pécs;
L Hejjel
Mt Jaberansari
G Jancso
University of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress can generate a mass of oxygen free radicals (OFR) in the cells, and these OFRs can induce several acute and chronic symptoms and diseases. If the amount of the generated OFRs overwhelms the antioxidant capacity of the cells, the pathophysiological changes may lead to the death of the cell or the development of chronic degenerative diseases.The phenomenon of ischemic preconditioning has demonstrated the important role of these aggressive and harmful molecules in the endogenous adaptation mechanism of the cells to oxidative stress. After sublethal oxidative stress - mild ischemic insult - the resulting development of a few OFRs can stimulate the intracellular signal-transduction cascade of ischemic preconditioning and, through the induction of severe transcription factors, new antioxidant enzymes and heat shock proteins will be synthesized. These newly synthesized proteins will protect the cellagainst another, more serious oxidative insult in the future.

Indexed as

Endogenous adaptationFree radicalsIschemic preconditioningSignal transduction

Identifiers

PMID19641690
PMCPMC2716256
OpenAlexW2184912343

What OpenQuestion holds

Textmetadata
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.