Evidence map›Paper›PMID 30392791›Full record

ReviewChest2019

Lung Repair and Regeneration in ARDS: Role of PECAM1 and Wnt Signaling.

Jesús Villar, Haibo Zhang, Arthur S Slutsky

Open access · bronzeAbstract readReview
In one paragraph

Review in Chest, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
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  17. Review
  18. Regenerative Signatures in BAL of Acute Respiratory Distress Syndrome.American journal of respiratory cell and molecular biology · 2024
    Article
  19. Article
  20. Article

26 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Jesús VillarCIBER de Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain; Multidisciplinary Organ Dysfunction Evaluation Research Network, Research Unit, Hospital Universitario Dr Negrin, Las Palmas de Gran Canaria, Spain; Keenan Research Center for Biomedical Sciences at the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Canada.
Haibo ZhangKeenan Research Center for Biomedical Sciences at the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Canada; Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Canada; Department of Anesthesia and Department of Physiology, University of Toronto, Toronto, Canada.
Arthur S SlutskyKeenan Research Center for Biomedical Sciences at the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Canada; Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Canada. Electronic address: slutskya@smh.ca.
St. Michael's Hospital · CAHospital Universitario de Gran Canaria Doctor Negrín · ES

Funding

CIHR FDN143285
6 · The paper itself

Abstract

ARDS is an acute inflammatory pulmonary process triggered by severe pulmonary and systemic insults to the alveolar-capillary membrane. This causes increased vascular permeability and the development of interstitial and alveolar protein-rich edema, leading to acute hypoxemic respiratory failure. Supportive treatment includes the use of lung-protective ventilatory strategies that decrease the work of breathing, can improve oxygenation, and minimize ventilator-induced lung injury. Despite substantial advances in supportive measures, there are no specific pharmacologic treatments for ARDS, and the overall hospital mortality rate remains about 40% in most series. The pathophysiology of ARDS involves interactions among multiple mechanisms, including immune cell infiltration, cytokine storm, alveolar-capillary barrier disruption, cell apoptosis, and the development of fibrosis. Here we review some new developments in the molecular basis of lung injury, with a focus on possible novel pharmacologic interventions aimed at improving the outcomes of patients with ARDS. Our focus is on platelet-endothelial cell adhesion molecule-1, which contributes to the maintenance and restoration of vascular integrity following barrier disruption. We also highlight the wingless-related integration site signaling pathway, which appears to be a central mechanism for lung healing as well as for fibrotic development.

Indexed as

Lung InjuryRespiratory Distress SyndromeHumansLungPlatelet Endothelial Cell Adhesion Molecule-1Pulmonary FibrosisRegenerationWnt Signaling PathwayPlatelet Endothelial Cell Adhesion Molecule-1endothelial injurymechanical ventilationplatelet-endothelial cell adhesion moleculepulmonary fibrosisventilator-induced lung injurywingless-related integration site

Identifiers

PMID30392791
PMCPMC6435939
OpenAlexW2898394729

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.