Evidence map›Paper›PMID 34997404›Full record

ArticleAngiogenesis2022

PHD2 deletion in endothelial or arterial smooth muscle cells reveals vascular cell type-specific responses in pulmonary hypertension and fibrosis.

Harri Elamaa, Mika Kaakinen, Marjut Nätynki, Zoltan Szabo, Veli-Pekka Ronkainen, Ville Äijälä, Joni M Mäki, Risto Kerkelä, Johanna Myllyharju, Lauri Eklund

Open access · hybridAbstract read
In one paragraph

Article in Angiogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. PHD1-3 oxygen sensors in vivo-lessons learned from gene deletions.Pflugers Archiv : European journal of physiology · 2024
    Review
  5. Article
  6. A Novel Animal Model for Pulmonary Hypertension: Lung Endothelial-Specific Deletion ofJournal of respiratory biology and translational medicine · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. The role of the cytoskeleton in fibrotic diseases.Frontiers in cell and developmental biology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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 3 institutions in 1 country.

Harri Elamaa *Oulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Mika Kaakinen *Oulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Marjut NätynkiOulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Zoltan SzaboBiocenter Oulu, University of Oulu, Oulu, Finland.
Veli-Pekka RonkainenBiocenter Oulu, University of Oulu, Oulu, Finland.
Ville ÄijäläOulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Joni M MäkiOulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Risto KerkeläBiocenter Oulu, University of Oulu, Oulu, Finland.
Johanna MyllyharjuOulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Lauri EklundOulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland. lauri.eklund@oulu.fi.ORCID 0000-0002-3177-7504
University of Oulu · FIOulu University Hospital · FIOulu University of Applied Sciences · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia plays an important regulatory role in the vasculature to adjust blood flow to meet metabolic requirements. At the level of gene transcription, the responses are mediated by hypoxia-inducible factor (HIF) the stability of which is controlled by the HIF prolyl 4-hydroxylase-2 (PHD2). In the lungs hypoxia results in vasoconstriction, however, the pathophysiological relevance of PHD2 in the major arterial cell types; endothelial cells (ECs) and arterial smooth muscle cells (aSMCs) in the adult vasculature is incompletely characterized. Here, we investigated PHD2-dependent vascular homeostasis utilizing inducible deletions of PHD2 either in ECs (Phd2

Indexed as

Hypertension, PulmonaryAnimalsArteriesEndothelial CellsFibrosisHypoxiaHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesMiceMyocytes, Smooth MuscleProlyl HydroxylasesHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesProlyl HydroxylasesBasement membraneEndothelial cellExtracellular matrixFibrosisHypoxiaPulmonary hypertensionSmooth muscle cell

Identifiers

PMID34997404
PMCPMC9054891
OpenAlexW4205363332

What OpenQuestion holds

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LicenceCC BY
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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.