Evidence map›Paper›PMID 35441845›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2022

Nets, pulmonary arterial hypertension, and thrombo-inflammation.

Luís Pedro Baptista de Barros Ribeiro Dourado, Mário Santos, Daniel Moreira-Gonçalves

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2022. 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
2.2field-weighted citation impact, top 11% 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, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
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  6. Article
  7. Article
  8. Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Article
  11. Article
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  14. 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

3 authors at 1 institution in 1 country.

Luís Pedro Baptista de Barros Ribeiro DouradoUnIC, Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Alameda Professor Hernâni Monteiro, 4200-319, Porto, Portugal. luisdourado17@gmail.com.ORCID 0000-0002-7918-6842
Mário SantosCardiology Department, Hospital Santo António, Centro Hospitalar Universitário do Porto, Largo do Prof. Abel Salazar, 4099-001, Porto, Portugal.
Daniel Moreira-GonçalvesCIAFEL, Faculty of Sport, University of Porto, R. Dr. Plácido da Costa 91, 4200-450, Porto, Portugal.
Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a progressive and fatal vascular disease in which high blood pressure in the pulmonary artery and remodeling of the pulmonary vasculature ensues. This disorder is characterized by the presence of thrombotic lesions, resulting from chronic platelet, coagulation factors, and endothelium activation, which translate into platelet aggregation, vasoconstriction, and medial thickening. Neutrophil extracellular traps (NETs), a network of chromatin and cytoplasmatic enzymes (myeloperoxidase and neutrophil elastase) forming after neutrophil programmed cell death, were described in multiple cardiovascular diseases as thrombotic mediators, by creating a scaffold or by surface receptor interaction. In this review, we analyze the possible involvement of NETs in PAH, to enlighten future studies to explore this hypothesis. NETs may have a determining role in pulmonary hypertension through activation of platelets and endothelial cells. Simultaneously, NETosis may be induced by endothelial signaling and/or cell-cell interaction between platelets and primed neutrophils, creating a positive feedback loop. Confirming its role in the pathophysiology and prognosis of PAH may represent a new opportunity to explore new therapeutic options. KEY MESSAGES: Thrombosis and innate immunity are relevant axes in PAH. Patients with PAH display elevated levels of NETs. NETs could activate platelets/endothelium with proliferative and thrombotic effects. Activated platelets and endothelium could contribute to NETosis. NETs could open new therapy research avenues.

Indexed as

Extracellular TrapsPulmonary Arterial HypertensionThrombosisEndothelial CellsFamilial Primary Pulmonary HypertensionHumansInflammationNeutrophilsReceptor Protein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesInnate immunityNeutrophilNeutrophil extracellular trapsPulmonary arterial hypertensionThrombosis

Identifiers

PMID35441845
OpenAlexW4224222103

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.