Evidence map›Paper›PMID 23662201›Full record

ArticlePulmonary circulation2013

Anticipated classes of new medications and molecular targets for pulmonary arterial hypertension.

Nicholas W Morrell, Stephen L Archer, Albert Defelice, Steven Evans, Monica Fiszman, Thomas Martin, Muriel Saulnier, Marlene Rabinovitch, Ralph Schermuly, Duncan Stewart and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Pulmonary circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Zinc-mediated Inhibition of Soluble Epoxide Hydrolase Promotes Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Anticipated pharmacological role of Aviptadil on COVID-19.Environmental science and pollution research international · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. 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

13 authors at 12 institutions in 7 countries.

Nicholas W MorrellDepartment of Medicine, University of Cambridge, UK.
Stephen L Archer
Albert Defelice
Steven Evans
Monica Fiszman
Thomas Martin
Muriel Saulnier
Marlene Rabinovitch
Ralph Schermuly
Duncan Stewart
Hubert Truebel
Gennyne Walker
Kurt R Stenmark
United States Food and Drug Administration · USBayer (Germany) · DECenter for Drug Evaluation and Research · USGilead Sciences (United States) · USNovartis (Switzerland) · CHOttawa Hospital · CAPfizer (United States) · USUniversities of Giessen and Marburg Lung Center · DEUniversity of Cambridge · GBUniversity of Chicago · USUniversity of Colorado Hospital · USUniversity of Giessen · DE

Funding

Pulmonary Hypertension in Genetically Modified MiceR01HL074186 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2004 to 2022
$10.4M
The BMP-PPARy Axis and Pulmonary HypertensionR01HL087118 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2008 to 2022
$7.2M
Fibroblasts and Mononuclear Fibrogenic Cells Drive Right Ventricular Pulmonary ArR01HL114887 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BULL, TODD M, BUTTRICK, PETER N. · 2012 to 2016
$3.4M
O2 sensing in the human and rabbit ductus arteriosus.R01HL071115 · NHLBI · UNIVERSITY OF CHICAGO · PI ARCHER, STEPHEN L · 2004 to 2015
$3.1M
The Role of DRP-1 and Mitochondrial Fission in Pulmonary Arterial HypertensionR01HL113003 · NHLBI · QUEEN'S UNIVERSITY AT KINGSTON · PI ARCHER, STEPHEN L · 2013 to 2016
$1.1M
British Heart Foundation RG/13/4/30107NHLBI NIH HHS R01 HL071115NHLBI NIH HHS R01 HL074186NHLBI NIH HHS R01 HL087118NHLBI NIH HHS R01 HL113003NHLBI NIH HHS R01 HL114887
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) remains a life-limiting condition with a major impact on the ability to lead a normal life. Although existing therapies may improve the outlook in some patients there remains a major unmet need to develop more effective therapies in this condition. There have been significant advances in our understanding of the genetic, cell and molecular basis of PAH over the last few years. This research has identified important new targets that could be explored as potential therapies for PAH. In this review we discuss whether further exploitation of vasoactive agents could bring additional benefits over existing approaches. Approaches to enhance smooth muscle cell apotosis and the potential of receptor tyrosine kinase inhibition are summarised. We evaluate the role of inflammation, epigenetic changes and altered glycolytic metabolism as potential targets for therapy, and whether inherited genetic mutations in PAH have revealed druggable targets. The potential of cell based therapies and gene therapy are also discussed. Potential candidate pathways that could be explored in the context of experimental medicine are identified.

Indexed as

apoptosiscellular mechanismsepigeneticsgeneticsinflammationmetabolismpulmonary arterial hypertensiontyrosine kinase inhibition

Identifiers

PMID23662201
PMCPMC3641734
OpenAlexW2036903679

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.