Evidence map›Paper›PMID 23341966›Full record

ArticlePloS one2013

Endothelial progenitor cells in the pathogenesis of idiopathic pulmonary fibrosis: an evolving concept.

Foteini Malli, Angela Koutsokera, Efrosini Paraskeva, Epaminondas Zakynthinos, Maria Papagianni, Dimosthenes Makris, Irene Tsilioni, Paschalis Adam Molyvdas, Konstantinos I Gourgoulianis, Zoe Daniil

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Antifibrotic and Regenerative Effects of Treamid in Pulmonary Fibrosis.International journal of molecular sciences · 2020
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. HIF1A up-regulates the ADORA2B receptor on alternatively activated macrophages and contributes to pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  18. Article
  19. Article
  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

10 authors at 1 institution in 1 country.

Foteini MalliRespiratory Medicine Department, School of Medicine, University of Thessaly, Larissa, Greece.
Angela Koutsokera
Efrosini Paraskeva
Epaminondas Zakynthinos
Maria Papagianni
Dimosthenes Makris
Irene Tsilioni
Paschalis Adam Molyvdas
Konstantinos I Gourgoulianis
Zoe Daniil
University of Thessaly · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdiopathic pulmonary fibrosis (IPF) has been associated with abnormal vascular remodeling. Bone marrow derived endothelial progenitor cells (EPCs) are considered to possess lung tissue repair and vascular remodeling properties.

objectivesThe study aimed to assess early EPCs levels and EPCs endogenous vascular endothelial growth factor (VEGF) expression in IPF. In order to examine alterations in the mobilization of EPCs from the bone marrow we measured plasma VEGF. MAIN

resultsTwenty-three patients with IPF and fifteen healthy subjects were included. The number of early EPCs colonies was markedly reduced in IPF patients vs controls (6.00±6.49 vs 49.68±16.73, respectively, p<0.001). EPCs were further decreased in patients presenting systolic pulmonary arterial pressure (sPAP)≥35 mmHg. The number of colonies per well correlated negatively with P((A-a))O(2) (r =  -0.750, p<0.001). Additionally, VEGF mRNA levels were significantly increased in IPF patients. There were no differences observed in VEGF plasma levels in IPF patients when compared to controls.

conclusionsThe current data suggest that inadequate levels of early EPCs may potentially contribute to suppressed repair and recovery of the damaged pulmonary endothelium and thereby may drive the sequence of events in profibrogenic direction. Increased VEGFmRNA levels in the clinical context of IPF may represent a compensatory mechanism to overcome reduced EPCs levels.

Indexed as

AgedBone Marrow CellsCell Culture TechniquesEndothelial CellsGene Expression RegulationHumansIdiopathic Pulmonary FibrosisMaleNeovascularization, PathologicRNA, MessengerSolubilityStem CellsVascular Endothelial Growth Factor ARNA, MessengerVascular Endothelial Growth Factor A

Identifiers

PMID23341966
PMCPMC3544914
OpenAlexW2074898234

What OpenQuestion 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 OpenQuestion graph.