Evidence map›Paper›PMID 28130261›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2017

Impact of thrombosis on pulmonary endothelial injury and repair following sepsis.

Colin E Evans, You-Yang Zhao

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Evaluation and Management of Sepsis in Pulmonary Hypertension.Journal of intensive care medicine · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Observational
  15. Editorial: Highlights in Thrombosis: 2021.Frontiers in cardiovascular medicine · 2022
    Article
  16. Article
  17. Article
  18. Observational
  19. Article
  20. Observational
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.

Colin E EvansDepartment of Pharmacology, University of Illinois at Chicago, College of Medicine, Chicago, Illinois; and.
You-Yang ZhaoDepartment of Pharmacology, University of Illinois at Chicago, College of Medicine, Chicago, Illinois; and yyzhao@uic.edu.
University of Illinois Chicago · US

Funding

Trpm2 Regulation of Phagocyte Bactericidal Activity and Resolution of Lung InjuryP01HL077806 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2005 to 2019
$27.0M
Novel mechanisms of obliterative pulmonary vascular remodeling and sever pulmonary arterial hypertensionR01HL133951 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2016 to 2024
$4.9M
Repair mechanisms of sepsis induced endothelial dysfunction and lung injuryR01HL125350 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B., ZHAO, YOU-YANG · 2014 to 2018
$3.2M
Novel Signalings and Molecular Targets Of Endothelial Regeneration In Aging LungR01HL123957 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2014 to 2018
$2.0M
NHLBI NIH HHS P01 HL077806NHLBI NIH HHS R01 HL125350NHLBI NIH HHS R01 HL133951
6 · The paper itself

Abstract

The prevailing morbidity and mortality in sepsis are largely due to multiple organ dysfunction (MOD), most commonly lung injury, as well as renal and cardiac dysfunction. Despite recent advances in defining many aspects of the pathogenesis of sepsis-related MOD, including acute respiratory distress syndrome (ARDS), there are currently no effective pharmacological or cell-based treatments for the disease. Human and animal studies have shown that pulmonary thrombosis is common in sepsis-induced ARDS, and preclinical studies have shown that anticoagulation may improve outcome following sepsis challenge. The potential beneficial effect of anticoagulation on outcome is unconvincing in clinical studies, however, and these discrepancies may arise from the multiple and sometimes opposing actions of thrombosis on the pulmonary endothelium following sepsis. It has been suggested, for example, that mild pulmonary thrombosis prevents escape of bacterial infection into the circulation, while severe thrombosis causes hypoxia and results in pulmonary endothelial damage. Evidence from both human and animal studies has demonstrated the key role of microvascular leakage in determining the outcome of sepsis. In this review, we describe thrombosis-dependent mechanisms that regulate pulmonary endothelial injury and repair following sepsis, including activation of the coagulation cascade by tissue factor and stimulation of vascular repair by hypoxia-inducible factors. Targeting such mechanisms through anticoagulant, anti-inflammatory, and reparative methods may represent a novel approach for the treatment of septic patients.

Indexed as

Wound HealingAnimalsEndothelium, VascularHumansLung InjuryModels, BiologicalSepsisThrombosisendotheliuminjurylungrepairsepsisthrombosis

Identifiers

PMID28130261
PMCPMC5407094
OpenAlexW2583053155

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.