Evidence map›Paper›PMID 28447104›Full record

ReviewCellular and molecular life sciences : CMLS2017

BMP type II receptor as a therapeutic target in pulmonary arterial hypertension.

Mar Orriols, Maria Catalina Gomez-Puerto, Peter Ten Dijke

Erratum issuedOpen access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Targeted delivery ofActa pharmaceutica Sinica. B · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. The pharmaco-epigenetics of hypertension: a focus on microRNA.Molecular and cellular biochemistry · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Mar OrriolsDepartment of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, Leiden, The Netherlands.
Maria Catalina Gomez-PuertoDepartment of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, Leiden, The Netherlands.
Peter Ten DijkeDepartment of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, Leiden, The Netherlands. p.ten_dijke@lumc.nl.
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a chronic disease characterized by a progressive elevation in mean pulmonary arterial pressure. This occurs due to abnormal remodeling of small peripheral lung vasculature resulting in progressive occlusion of the artery lumen that eventually causes right heart failure and death. The most common cause of PAH is inactivating mutations in the gene encoding a bone morphogenetic protein type II receptor (BMPRII). Current therapeutic options for PAH are limited and focused mainly on reversal of pulmonary vasoconstriction and proliferation of vascular cells. Although these treatments can relieve disease symptoms, PAH remains a progressive lethal disease. Emerging data suggest that restoration of BMPRII signaling in PAH is a promising alternative that could prevent and reverse pulmonary vascular remodeling. Here we will focus on recent advances in rescuing BMPRII expression, function or signaling to prevent and reverse pulmonary vascular remodeling in PAH and its feasibility for clinical translation. Furthermore, we summarize the role of described miRNAs that directly target the BMPR2 gene in blood vessels. We discuss the therapeutic potential and the limitations of promising new approaches to restore BMPRII signaling in PAH patients. Different mutations in BMPR2 and environmental/genetic factors make PAH a heterogeneous disease and it is thus likely that the best approach will be patient-tailored therapies.

Indexed as

Signal TransductionAnimalsBone Morphogenetic Protein Receptors, Type IIDisease Models, AnimalEndothelial CellsGene Expression RegulationGenetic TherapyGene Transfer TechniquesHumansHypertension, PulmonaryMicroRNAsMolecular Targeted TherapyMuscle, Smooth, VascularPulmonary ArterySmad ProteinsBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IIMicroRNAsSmad ProteinsEndothelial cellInflammationSignal transductionVascular remodeling and autophagyVascular smooth muscle cell

Identifiers

PMID28447104
PMCPMC5501910
OpenAlexW2609733517

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.