Evidence map›Paper›PMID 32733669›Full record

ArticlePulmonary circulation

Targeting translational read-through of premature termination mutations in

Lu Long, Xudong Yang, Mark Southwood, Stephen Moore, Alexi Crosby, Paul D Upton, Benjamin J Dunmore, Nicholas W Morrell

Open access · goldAbstract read
In one paragraph

Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Clinical Updates in Pulmonary Hypertension.Reviews in cardiovascular medicine · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Nonsense suppression therapies in human genetic diseases.Cellular and molecular life sciences : CMLS · 2021
    Review
  10. Review
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

8 authors at 2 institutions in 1 country.

Lu LongDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Xudong YangDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Mark SouthwoodPathology Research, Royal Papworth Hospital NHS Foundation Trust, Cambridge, UK.
Stephen MooreDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Alexi CrosbyDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Paul D UptonDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Benjamin J DunmoreDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Nicholas W MorrellDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
University of Cambridge · GBPapworth Hospital NHS Foundation Trust · GB

Funding

British Heart Foundation CH/09/001/25945British Heart Foundation RG/19/3/34265
6 · The paper itself

Abstract

Pulmonary arterial hypertension is a fatal disorder of the lung circulation in which accumulation of vascular cells progressively obliterates the pulmonary arterioles. This results in sustained elevation in pulmonary artery pressure leading eventually to right heart failure. Approximately, 80% of familial and 20% of sporadic idiopathic pulmonary arterial hypertension cases are caused by mutations in the bone morphogenetic protein receptor type 2 (BMPR2). Nonsense mutations in

Indexed as

mutationspulmonary endotheliumtranslational research

Identifiers

PMID32733669
PMCPMC7372630
OpenAlexW3033977032

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.