Evidence map›Paper›PMID 21401517›Full record

ReviewCurrent pharmaceutical biotechnology2011

Therapeutic modulation of coagulation and fibrinolysis in acute lung injury and the acute respiratory distress syndrome.

Sara C Sebag, Julie A Bastarache, Lorraine B Ware

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Current pharmaceutical biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04558125 (Low-Dose Tenecteplase in Covid-19 Patients With Acute Pulmonary Embolism), which is not on this map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 16% 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.

NCT04558125 phase4terminatednot on this mapstarted 2020, after this paper: background citation

Low-Dose Tenecteplase in Covid-19 Patients With Acute Pulmonary Embolism: A Randomized, Double-Blind, Placebo-Controlled Trial

TypeinterventionalSponsorCedars-Sinai Medical CenterRan2020 to 2021Enrolled2ConditionsPulmonary Embolism, COVIDArmsTNKase, Placebo, Enoxaparin
3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Dexamethasone inhibits endotoxin-induced coagulopathy in human lungs.Journal of thrombosis and haemostasis : JTH · 2016
    Trial
  4. Trial
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  16. Article
  17. SARS-CoV-2 pathogenesis.Nature reviews. Microbiology · 2022
    Review
  18. Review
  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

3 authors at 1 institution in 1 country.

Sara C SebagDepartment of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, T1218 MCN, 1161 21st Avenue S. Nashville, TN 37232-2650, USA.
Julie A Bastarache
Lorraine B Ware
Vanderbilt University Medical Center · US

Funding

Clinical and Translational Training Program in Pulmonary MedicineT32HL087738 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Lorraine B Ware · 2007 to 2026
$7.0M
Biomarker Profiles in the Diagnosis/Prognosis of ARDSU01HL081332 · NHLBI · VANDERBILT UNIVERSITY · PI WARE, LORRAINE B · 2005 to 2008
$6.0M
Tissue Factor Mediated Fibrin Deposition in Acute Lung InjuryK08HL090785 · NHLBI · VANDERBILT UNIVERSITY · PI BASTARACHE, JULIE ANNE · 2009 to 2013
$629k
NHLBI NIH HHS K08 HL090785NHLBI NIH HHS T32 HL087738NHLBI NIH HHS U01 HL081332
6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are characterized by excessive intraalveolar fibrin deposition, driven, at least in part by inflammation. The imbalance between activation of coagulation and inhibition of fibrinolysis in patients with ALI/ARDS favors fibrin formation and appears to occur both systemically and in the lung and airspace. Tissue factor (TF), a key mediator of the activation of coagulation in the lung, has been implicated in the pathogenesis of ALI/ARDS. As such, there have been numerous investigations modulating TF activity in a variety of experimental systems in order to develop new therapeutic strategies for ALI/ARDS. This review will summarize current understanding of the role of TF and other proteins of the coagulation cascade as well the fibrinolysis pathway in the development of ALI/ARDS with an emphasis on the pathways that are potential therapeutic targets. These include the TF inhibitor pathway, the protein C pathway, antithrombin, heparin, and modulation of fibrinolysis through plasminogen activator- 1 (PAI-1) or plasminogen activators (PA). Although experimental studies show promising results, clinical trials to date have proven unsuccessful in improving patient outcomes. Modulation of coagulation and fibrinolysis has complex effects on both hemostasis and inflammatory pathways and further studies are needed to develop new treatment strategies for patients with ALI/ARDS.

Indexed as

Acute Lung InjuryAnimalsAntithrombinsBlood CoagulationFactor VIIaHeparinHumansInflammationProtein CRecombinant ProteinsRespiratory Distress SyndromeThromboplastinAntithrombinsFactor VIIaHeparinProtein Crecombinant FVIIaRecombinant ProteinsThromboplastin

Identifiers

PMID21401517
PMCPMC3893117
OpenAlexW2131228216

What OpenQuestion holds

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Registered trials

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.