Evidence map›Paper›PMID 23202940›Full record

ReviewInternational journal of molecular sciences2012

Disease progression mediated by egr-1 associated signaling in response to oxidative stress.

Judith-Irina Pagel, Elisabeth Deindl

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed.

  1. Trial
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  4. Transcription-based comparison ofMicrobiology spectrum · 2026
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  10. Batokine in Central Nervous System Diseases.Molecular neurobiology · 2023
    Review
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  16. International journal of molecular sciences · 2022
    Article
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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

2 authors.

Judith-Irina PagelWalter-Brendel-Centre of Experimental Medicine, Ludwig-Maximilians-University, Munich D-81377, Germany. judith.pagel@med.uni-muenchen.de.
Elisabeth Deindl

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When cellular reducing enzymes fail to shield the cell from increased amounts of reactive oxygen species (ROS), oxidative stress arises. The redox state is misbalanced, DNA and proteins are damaged and cellular transcription networks are activated. This condition can lead to the initiation and/or to the progression of atherosclerosis, tumors or pulmonary hypertension; diseases that are decisively furthered by the presence of oxidizing agents. Redox sensitive genes, like the zinc finger transcription factor early growth response 1 (Egr-1), play a pivotal role in the pathophysiology of these diseases. Apart from inducing apoptosis, signaling partners like the MEK/ERK pathway or the protein kinase C (PKC) can activate salvage programs such as cell proliferation that do not ameliorate, but rather worsen their outcome. Here, we review the currently available data on Egr-1 related signal transduction cascades in response to oxidative stress in the progression of epidemiologically significant diseases. Knowing the molecular pathways behind the pathology will greatly enhance our ability to identify possible targets for the development of new therapeutic strategies.

Indexed as

Oxidative StressAtherosclerosisEarly Growth Response Protein 1HerpesviridaeHerpesviridae InfectionsHumansHypertension, PulmonaryNADPH OxidasesProtein Kinase CPulmonary FibrosisEarly Growth Response Protein 1NADPH OxidasesProtein Kinase C

Identifiers

PMID23202940
PMCPMC3497314

What OpenQuestion holds

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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.