Evidence map›Paper›PMID 33535429›Full record

ReviewInternational journal of molecular sciences2021

The Contribution of the Urokinase Plasminogen Activator and the Urokinase Receptor to Pleural and Parenchymal Lung Injury and Repair: A Narrative Review.

Torry A Tucker, Steven Idell

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Association ofInternational journal of molecular sciences · 2022
    Article
  11. Article
  12. Article
  13. Update on Novel Targeted Therapy for Pleural Organization and Fibrosis.International journal of molecular sciences · 2022
    Review
  14. 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

2 authors at 1 institution in 1 country.

Torry A TuckerThe Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Steven IdellThe Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
The University of Texas Health Science Center at Tyler · US

Funding

Myocardin in the pathogenesis of pleural remodelingR01HL142853 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI IDELL, STEVEN, IKEBE, MITSUO · 2019 to 2022
$1.9M
Fibrinolytic Proteases, meso-mesenchymal transition and pleural remodelingR01HL130133 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI TUCKER, TORRY ALLE · 2017 to 2021
$1.8M
Control of fibrosing lung disease by p53-miR-34a-targeted therapeuticsR01HL133067 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI SHETTY, SREERAMA · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL130133NHLBI NIH HHS R01 HL142853NIH HHS HHSN268201100014CNIH HHS HL121841NIH HHS HL130402NIH HHS HL14285301NIH HHS HL154103NIH HHS R01HL130133NIH HHS R01HL133067NIH HHS U54 TR002804
6 · The paper itself

Abstract

Pleural and parenchymal lung injury have long been characterized by acute inflammation and pathologic tissue reorganization, when severe. Although transitional matrix deposition is a normal part of the injury response, unresolved fibrin deposition can lead to pleural loculation and scarification of affected areas. Within this review, we present a brief discussion of the fibrinolytic pathway, its components, and their contribution to injury progression. We review how local derangements of fibrinolysis, resulting from increased coagulation and reduced plasminogen activator activity, promote extravascular fibrin deposition. Further, we describe how pleural mesothelial cells contribute to lung scarring via the acquisition of a profibrotic phenotype. We also discuss soluble uPAR, a recently identified biomarker of pleural injury, and its diagnostic value in the grading of pleural effusions. Finally, we provide an in-depth discussion on the clinical importance of single-chain urokinase plasminogen activator (uPA) for the treatment of loculated pleural collections.

Indexed as

Acute DiseaseAnimalsBiomarkersBlood CoagulationEpitheliumFibrinFibrinolysisHumansInflammationLungLung InjuryPleuraPleural EffusionReceptors, Urokinase Plasminogen ActivatorThrombolytic TherapyUrokinase-Type Plasminogen ActivatorBiomarkersFibrinPLAUR protein, humanReceptors, Urokinase Plasminogen ActivatorUrokinase-Type Plasminogen Activatoracute lung injury and repair and pleural injury and pleural organizationfibrinolysisplasminogen activator inhibitor-1urokinase plasminogen activatorurokinase plasminogen activator receptor

Identifiers

PMID33535429
PMCPMC7867090
OpenAlexW3127969920

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.