Evidence map›Paper›PMID 35625405›Full record

ArticleBiology2022

EGR1 Is Implicated in Right Ventricular Cardiac Remodeling Associated with Pulmonary Hypertension.

Maria Laggner, Felicitas Oberndorfer, Bahar Golabi, Jonas Bauer, Andreas Zuckermann, Philipp Hacker, Irene Lang, Nika Skoro-Sajer, Christian Gerges, Shahrokh Taghavi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

11 citing papers in PubMed, 29 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

14 authors at 2 institutions in 1 country.

Maria LaggnerDepartment of Thoracic Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Felicitas OberndorferClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Bahar GolabiDepartment of Dermatology, Medical University of Vienna, 1090 Vienna, Austria.
Jonas BauerDepartment of Thoracic Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-3328-7795
Andreas ZuckermannDepartment of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.
Philipp HackerDepartment of Oral and Maxillofacial Surgery, University Hospital St. Poelten, 3100 St. Poelten, Austria.
Irene LangDepartment of Medicine II, Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-0485-2692
Nika Skoro-SajerDepartment of Medicine II, Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.
Christian GergesDepartment of Medicine II, Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria.
Shahrokh TaghaviDepartment of Thoracic Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Peter JakschDepartment of Thoracic Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-4635-3242
Michael MildnerDepartment of Dermatology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-6892-925X
Hendrik Jan AnkersmitDepartment of Thoracic Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Bernhard MoserDepartment of Thoracic Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-6037-5475
Medical University of Vienna · ATUniversity of Applied Sciences St Pölten · AT

Funding

Austrian Research Promotion Agency 862068
6 · The paper itself

Abstract

backgroundPulmonary hypertension (PH) is a vasoconstrictive disease characterized by elevated mean pulmonary arterial pressure (mPAP) at rest. Idiopathic pulmonary arterial hypertension (iPAH) and chronic thromboembolic pulmonary hypertension (CTEPH) represent two distinct subtypes of PH. Persisting PH leads to right ventricular (RV) hypertrophy, heart failure, and death. RV performance predicts survival and surgical interventions re-establishing physiological mPAP reverse cardiac remodeling. Nonetheless, a considerable number of PH patients are deemed inoperable. The underlying mechanism(s) governing cardiac regeneration, however, remain largely elusive.

methodsIn a longitudinal approach, we profiled the transcriptional landscapes of hypertrophic RVs and recovered hearts 3 months after surgery of iPAH and CTEPH patients.

resultsGenes associated with cellular responses to inflammatory stimuli and metal ions were downregulated, and cardiac muscle tissue development was induced in iPAH after recovery. In CTEPH patients, genes related to muscle cell development were decreased, and genes governing cardiac conduction were upregulated in RVs following regeneration. Intriguingly, early growth response 1 (

conclusionOur findings improved our understanding of the molecular events driving reverse cardiac remodeling following surgery. EGR1 might represent a promising candidate for targeted therapy of PH patients not eligible for surgical treatment.

Indexed as

chronic thromboembolic pulmonary hypertensionEGR1idiopathic pulmonary arterial hypertensionlung transplantationpulmonary endarterectomypulmonary hypertensionreverse right ventricular remodelingright ventricular hypertrophy

Identifiers

PMID35625405
PMCPMC9138384
OpenAlexW4281765894

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.