Evidence map›Paper›PMID 21761156›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2011

From oncoproteins/tumor suppressors to microRNAs, the newest therapeutic targets for pulmonary arterial hypertension.

Roxane Paulin, Audrey Courboulin, Marjorie Barrier, Sébastien Bonnet

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Biological Bases of Group 2 Pulmonary Hypertension.International journal of molecular sciences · 2019
    Review
  4. Article
  5. Article
  6. Article
  7. Mitochondrial HSP90 Accumulation Promotes Vascular Remodeling in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2018
    Article
  8. Article
  9. Translating Research into Improved Patient Care in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2017
    Review
  10. Article
  11. Dysregulation of microRNA-214 and PTEN contributes to the pathogenesis of hypoxic pulmonary hypertension.International journal of chronic obstructive pulmonary disease · 2017
    Article
  12. Review
  13. Molecular mechanisms of pulmonary arterial remodeling.Molecular medicine (Cambridge, Mass.) · 2014
    Review
  14. Article
  15. Review
  16. Regulation of ca(2+) signaling in pulmonary hypertension.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013
    Article
  17. Review
  18. Review
  19. Looking to the future: a new decade of pulmonary arterial hypertension therapy.European respiratory review : an official journal of the European Respiratory Society · 2011
    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

4 authors at 2 institutions in 1 country.

Roxane PaulinDepartment of Medicine, Laval University, Centre de Recherche du CHUQ, Hôtel-Dieu de Québec, Québec, QC, Canada.
Audrey Courboulin
Marjorie Barrier
Sébastien Bonnet
Hôtel-Dieu de Québec · CAUniversité Laval · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a disease of the pulmonary vasculature characterized by constricted and remodeled pulmonary arteries. This phenomenon is associated with enhanced pulmonary artery smooth muscle cells proliferation and suppressed apoptosis, metabolism shift, inflammation, and several other features that are considered as hallmarks of cancer. Since oncogenes, tumor suppressors, and miRNAs are the major regulators of signaling in the cancer phenotype, we studied if the same type of regulation is operative in PAH. From the discovery of BMPR2 mutation in familial forms of PAH, oncogenic pathways activation like MAPK were identified. Recently, the Src/STAT3/Pim1 axis was also described as playing a critical role in PAH pathogenesis. Moreover, through the down-regulation of miR-204, STAT3 enhances a positive feedback loop sustaining its own activation, showing that miRNA regulation is critical in PAH. Taken together, targeting oncoproteins or miRNAs appear as new therapeutic strategies for PAH. Several oncoprotein inhibitors are already in trials for cancer and could be soon available for PAH. Concerning miRNAs, the youth of this area makes therapies less achievable soon but not less interesting.

Indexed as

AnimalsApoptosisBone Morphogenetic Protein Receptors, Type IICell ProliferationDown-RegulationGenetic Diseases, InbornHumansHypertension, PulmonaryMAP Kinase Signaling SystemMicroRNAsMuscle, Smooth, VascularMutationMyocytes, Smooth MuscleNeoplasmsProto-Oncogene Proteins c-pim-1src-Family KinasesBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IIMicroRNAsMIRN204 microRNA, humanPIM1 protein, humanProto-Oncogene Proteins c-pim-1src-Family KinasesSTAT3 protein, humanSTAT3 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID21761156
OpenAlexW1984147340

What OpenQuestion holds

Textmetadata
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.