Evidence map›Paper›PMID 36847444›Full record

ReviewAmerican journal of physiology. Cell physiology2023

The role of the alveolar epithelial glycocalyx in acute respiratory distress syndrome.

Alicia N Rizzo, Eric P Schmidt

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  8. Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025
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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.

Alicia N RizzoDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States.ORCID 0000-0001-9289-4635
Eric P SchmidtDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States.ORCID 0000-0002-7360-0504
Harvard University · US

Funding

Endothelial glycocalyx reconstitution during sepsisR01HL125371 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI LINHARDT, ROBERT J, SCHMIDT, ERIC PETER · 2014 to 2018
$3.4M
Epithelial glycocalyx degradation mediates surfactant dysfunction in acute respiratory distress syndromeF32HL162230 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI RIZZO, ALICIA N · 2022 to 2023
$121k
NHLBI NIH HHS F32 HL162230NHLBI NIH HHS L30 HL159703NHLBI NIH HHS R01 HL125371
6 · The paper itself

Abstract

The alveolar epithelial glycocalyx is a dense anionic layer of glycosaminoglycans (GAGs) and proteoglycans that lines the apical surface of the alveolar epithelium. In contrast to the pulmonary endothelial glycocalyx, which has well-established roles in vascular homeostasis and septic organ dysfunction, the alveolar epithelial glycocalyx is less understood. Recent preclinical studies demonstrated that the epithelial glycocalyx is degraded in multiple murine models of acute respiratory distress syndrome (ARDS), particularly those that result from inhaled insults (so-called "direct" lung injury), leading to shedding of GAGs into the alveolar airspaces. Epithelial glycocalyx degradation also occurs in humans with respiratory failure, as quantified by analysis of airspace fluid obtained from ventilator heat moisture exchange (HME) filters. In patients with ARDS, GAG shedding correlates with the severity of hypoxemia and is predictive of the duration of respiratory failure. These effects may be mediated by surfactant dysfunction, as targeted degradation of the epithelial glycocalyx in mice was sufficient to cause increased alveolar surface tension, diffuse microatelectasis, and impaired lung compliance. In this review, we describe the structure of the alveolar epithelial glycocalyx and the mechanisms underlying its degradation during ARDS. We additionally review the current state of knowledge regarding the attributable effect of epithelial glycocalyx degradation in lung injury pathogenesis. Finally, we address glycocalyx degradation as a potential mediator of ARDS heterogeneity, and the subsequent value of point-of-care quantification of GAG shedding to potentially identify patients who are most likely to respond to pharmacological agents aimed at attenuating glycocalyx degradation.

Indexed as

Lung InjuryRespiratory Distress SyndromeRespiratory InsufficiencyAnimalsGlycocalyxHumansLungMiceglycocalyxheparan sulfatelung injurymatrix metalloproteinasesurfactant

Identifiers

PMID36847444
PMCPMC10042597
OpenAlexW4322494976

What Socratic 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 Socratic graph.