Evidence map›Paper›PMID 26787464›Full record

ArticleFEBS letters2016

PDGF-dependent β-catenin activation is associated with abnormal pulmonary artery smooth muscle cell proliferation in pulmonary arterial hypertension.

Jack Takahashi, Mark Orcholski, Ke Yuan, Vinicio de Jesus Perez

Open access · bronzeAbstract read
In one paragraph

Article in FEBS letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  3. Article
  4. AFrontiers in cardiovascular medicine · 2024
    Article
  5. Transcriptomic Study on the Lungs of Broilers with Ascites Syndrome.Animals : an open access journal from MDPI · 2023
    Article
  6. Article
  7. MicroRNA miR-627-5p restrains pulmonary artery smooth muscle cell dysfunction by targeting MAP 2 K4 and PI3K/AKT signaling.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. [The Effects of Ginsenoside Compound K on PDGF-BB-Induced PASMCs Proliferation and Phenotypic Conversion of Pulmonary Arterial Smooth Muscle Cells].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    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

4 authors at 2 institutions in 1 country.

Jack TakahashiDivision of Pulmonary and Critical Care Medicine, Stanford, CA, USA.
Mark OrcholskiDivision of Pulmonary and Critical Care Medicine, Stanford, CA, USA.
Ke YuanDivision of Pulmonary and Critical Care Medicine, Stanford, CA, USA.
Vinicio de Jesus PerezDivision of Pulmonary and Critical Care Medicine, Stanford, CA, USA.
Cardiovascular Institute of the South · USStanford Medicine · US

Funding

The role of the Wnt/planar cell polarity pathway in pulmonary angiogenesisK08HL105884 · NHLBI · STANFORD UNIVERSITY · PI DE JESUS PEREZ, VINICIO A · 2012 to 2016
$701k
NHLBI NIH HHS K08 HL105884NHLBI NIH HHS K08 HL105884-01
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is characterized by excessive pulmonary arterial smooth muscle cells (PASMCs) growth, partially in response to PDGF-BB but whether this is dependent on β-catenin (βC) activation is unclear. Compared to healthy cells, PAH PASMCs demonstrate higher levels of proliferation both at baseline and with PDGF-BB that correlate with GSK3β dependent βC activation. We show that βC knockdown but not Wnt5a stimulation reduces PDGF-BB dependent growth and normalizes PAH PASMCs proliferation. These findings support that cross-talk between PDGF and Wnt signaling modulates PASMC proliferation and suggest that βC targeted therapies could treat abnormal vascular remodeling in PAH.

Indexed as

Wnt Signaling PathwayActive Transport, Cell NucleusAnticoagulantsBecaplerminbeta CateninCell ProliferationCells, CulturedFamilial Primary Pulmonary HypertensionGene Expression RegulationGenes, ReporterGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMuscle, Smooth, VascularPhosphorylationPromoter Regions, GeneticAnticoagulantsBecaplerminbeta CateninCTNNB1 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-sisRecombinant ProteinsWnt-5a ProteinWNT5A protein, humanWnt ProteinsPDGFpulmonary diseasepulmonary hypertensionsmooth muscle cellsvascular remodelingWnt signaling

Identifiers

PMID26787464
PMCPMC4722963
OpenAlexW2267472969

What OpenQuestion holds

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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.