Evidence map›Paper›PMID 27246590›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2016

Epigenetic mechanisms in pulmonary arterial hypertension: the need for global perspectives.

Prakash Chelladurai, Werner Seeger, Soni Savai Pullamsetti

Open access · diamondAbstract readReview
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Histone Methyl Transferase G9a/GLP-A Novel Avenue in Pulmonary Arterial Hypertension Treatment?American journal of respiratory cell and molecular biology · 2023
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. DNA Methylation and Histone Modification in Hypertension.International journal of molecular sciences · 2018
    Review
  20. Article
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

3 authors at 2 institutions in 1 country.

Prakash ChelladuraiMax-Planck-Institute for Heart and Lung Research, Dept of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), Bad Nauheim, Germany.
Werner SeegerMax-Planck-Institute for Heart and Lung Research, Dept of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), Bad Nauheim, Germany University of Giessen Lung Center (UGMLC), member of the German Center for Lung Research (DZL), Justus-Liebig University, Giessen, Germany.
Soni Savai PullamsettiMax-Planck-Institute for Heart and Lung Research, Dept of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), Bad Nauheim, Germany University of Giessen Lung Center (UGMLC), member of the German Center for Lung Research (DZL), Justus-Liebig University, Giessen, Germany soni.pullamsetti@mpi-bn.mpg.de.
Universities of Giessen and Marburg Lung Center · DEGerman Center for Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe and progressive disease, characterised by high pulmonary artery pressure that usually culminates in right heart failure. Recent findings of alterations in the DNA methylation state of superoxide dismutase 2 and granulysin gene loci; histone H1 levels; aberrant expression levels of histone deacetylases and bromodomain-containing protein 4; and dysregulated microRNA networks together suggest the involvement of epigenetics in PAH pathogenesis. Thus, PAH pathogenesis evidently involves the interplay of a predisposed genetic background, epigenetic state and injurious events. Profiling the genome-wide alterations in the epigenetic mechanisms, such as DNA methylation or histone modification pattern in PAH vascular cells, may explain the great variability in susceptibility and disease severity that is frequently associated with pronounced remodelling and worse clinical outcome. Moreover, the influence of genetic predisposition and the acquisition of epigenetic alterations in response to environmental cues in PAH progression and establishment has largely been unexplored on a genome-wide scale. In order to gain insights into the molecular mechanisms leading to the development of PAH and to design novel therapeutic strategies, high-throughput approaches have to be adopted to facilitate systematic identification of the disease-specific networks using next-generation sequencing technologies, the application of these technologies in PAH has been relatively trivial to date.

Indexed as

Chromatin Assembly and DisassemblyDNA MethylationEpigenesis, GeneticAnimalsAntihypertensive AgentsArterial PressureGene Regulatory NetworksGenetic Predisposition to DiseaseGenomicsHigh-Throughput Nucleotide SequencingHistone Deacetylase InhibitorsHumansHypertension, PulmonaryMolecular Targeted TherapyPhenotypePulmonary ArteryAntihypertensive AgentsHistone Deacetylase Inhibitors

Identifiers

PMID27246590
PMCPMC9487251
OpenAlexW2408851452

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.