Evidence map›Paper›PMID 30131961›Full record

ReviewFrontiers in medicine2018

The Role of Neutrophils and Neutrophil Elastase in Pulmonary Arterial Hypertension.

Shalina Taylor, Omar Dirir, Roham T Zamanian, Marlene Rabinovitch, A A Roger Thompson

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Synergistic and Antagonistic Mechanisms ofMolecules (Basel, Switzerland) · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
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  20. Review
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

5 authors at 2 institutions in 2 countries.

Shalina TaylorDepartment of Pediatrics, Stanford University School of Medicine, Stanford, CA, United States.
Omar DirirInfection, Immunity, and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Roham T ZamanianVera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University, Stanford, CA, United States.
Marlene RabinovitchDepartment of Pediatrics, Stanford University School of Medicine, Stanford, CA, United States.
A A Roger ThompsonInfection, Immunity, and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Stanford University · USUniversity of Sheffield · GB

Funding

The Cellular Response to Elafin in PAHP01HL108797 · NHLBI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2011 to 2021
$19.7M
The BMP-PPARy Axis and Pulmonary HypertensionR01HL087118 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2008 to 2022
$7.2M
Endothelial Injury, BMPR2 Dysfunction and Macrophage Activation Cause EndMT and PAHR01HL138473 · NHLBI · STANFORD UNIVERSITY · PI Mark Robert Nicolls, Marlene Rabinovitch · 2017 to 2026
$4.9M
Stanford Training Program in Lung BiologyT32HL129970 · NHLBI · STANFORD UNIVERSITY · PI CORNFIELD, DAVID N., NICOLLS, MARK ROBERT · 2016 to 2025
$3.2M
British Heart Foundation FS/18/13/33281Medical Research Council G0802255NHLBI NIH HHS P01 HL108797NHLBI NIH HHS R01 HL087118NHLBI NIH HHS R01 HL138473NHLBI NIH HHS T32 HL129970
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe vasculopathy characterized by the presence of fibrotic lesions in the arterial wall and the loss of small distal pulmonary arteries. The vasculopathy is accompanied by perivascular inflammation and increased protease levels, with neutrophil elastase notably implicated in aberrant vascular remodeling. However, the source of elevated elastase levels in PAH remains unclear. A major source of neutrophil elastase is the neutrophil, an understudied cell population in PAH. The principal function of neutrophils is to destroy invading pathogens by means of phagocytosis and NET formation, but proteases, chemokines, and cytokines implicated in PAH can be released by and/or prime and activate neutrophils. This review focuses on the contribution of inflammation to the development and progression of the disease, highlighting studies implicating neutrophils, neutrophil elastase, and other neutrophil proteases in PAH. The roles of cytokines, chemokines, and neutrophil elastase in the disease are discussed and we describe new insight into the role neutrophils potentially play in the pathogenesis of PAH.

Indexed as

neutrophil elastaseneutrophilspulmonary arterial hypertensionpulmonary hypertensionvascular remodeling

Identifiers

PMID30131961
PMCPMC6090899
OpenAlexW2885447280

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.