Evidence map›Paper›PMID 39619154›Full record

ReviewFrontiers in cardiovascular medicine2024

Early growth response-1, a dynamic conduit in cardiovascular disease.

Levon M Khachigian

Abstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2024. 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
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.

  1. Article
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  6. Review
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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

1 author.

Levon M KhachigianVascular Biology and Translational Research, Department of Pathology, Faculty of Medicine and Health, School of Biomedical Sciences, University of New South Wales, Sydney, NSW, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor, early growth response-1 (Egr-1) is the product of a prototypic immediate-early gene that plays an integral role in the pathogenesis of multiple cardiovascular diseases. Egr-1 has been linked with atherogenesis, myocardial ischemia-reperfusion injury, cardiac fibrosis and heart failure. Egr-1 expression is triggered by a host of factors including cytokines, hormones, growth factors, hyperglycaemia, biomechanical forces and oxygen deprivation. Egr-1 is a molecular conduit that links changes in the cellular environment with the inducible expression of genes whose products play a causative role in this inflammatory disease. It is rapidly synthesised, undergoes post-translational modification, interacts with a range of cofactors and drives gene expression. Studies in Egr-1 deficient mice, animal models using DNAzymes, RNA interference, oligodeoxynucleotide decoys, antisense oligonucleotides, and new insights provided by technologies such as single cell RNA sequencing, have shaped our understanding of the importance of Egr-1 in the initiation and progression of cardiovascular disease. This article describes Egr-1's role in various cardiovascular settings and discusses potential mechanisms of action. Given the range of conditions linked to Egr-1, this zinc finger protein may serve as a therapeutic target for intervention.

Indexed as

acute coronary syndromecardiovascular diseaseearly growth response-1EGR1vascular biology

Identifiers

PMID39619154
PMCPMC11605393

What Socratic holds

Textmetadata
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 Socratic graph.