Evidence map›Paper›PMID 42362731›Full record

ArticleScientific reports2026

Plasma heparan sulfate structural variation and phenotypic heterogeneity in pediatric Acute Respiratory Distress Syndrome.

Colin J Sallee, Aline B Maddux, Joseph A Hippensteel, Daniela Markovic, Zhangjie Wang, Jian Liu, Kaori Oshima, Robert P Richter, Andreas Schwingshackl, Peter M Mourani and 3 more

Abstract read
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In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Colin J SalleeDepartment of Pediatrics, Division of Pediatric Critical Care Medicine, David Geffen School of Medicine at University of California Los Angeles and Mattel Childrens Hospital, Los Angeles, CA, USA. csallee@mednet.ucla.edu.ORCID http://orcid.org/0000-0002-2834-2657
Aline B MadduxDepartment of Pediatrics, Section of Pediatric Critical Care, University of Colorado School of Medicine and Children's Hospital Colorado, Aurora, CO, USA.
Joseph A HippensteelDepartment of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Daniela MarkovicDepartments of Medicine and Computational Biology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA.
Zhangjie WangGlycan Therapeutics, Raleigh, NC, USA.
Jian LiuDivision of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Kaori OshimaDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Harvard Medical School and Massachusetts General Hospital, Boston, MA, USA.
Robert P RichterDepartment of Pediatrics, Division of Pediatric Critical Care Medicine, University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL, USA.
Andreas SchwingshacklDepartment of Pediatrics, Division of Pediatric Critical Care Medicine, David Geffen School of Medicine at University of California Los Angeles and Mattel Childrens Hospital, Los Angeles, CA, USA.
Peter M MouraniDepartment of Pediatrics, Division of Pediatric Critical Care Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
David ElashoffDepartments of Medicine and Computational Biology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA.
Eric P SchmidtDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Harvard Medical School and Massachusetts General Hospital, Boston, MA, USA.
Anil SapruDepartment of Pediatrics, Division of Pediatric Critical Care Medicine, David Geffen School of Medicine at University of California Los Angeles and Mattel Childrens Hospital, Los Angeles, CA, USA.

Funding

Endothelial glycocalyx reconstitution during sepsisR01HL125371 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI LINHARDT, ROBERT J, SCHMIDT, ERIC PETER · 2014 to 2018
$3.4M
Development of analytical methods for glycosaminoglycans from biological sourcesR44GM142304 · NIGMS · GLYCAN THERAPEUTICS CORPORATION · PI WANG, ZHANGJIE · 2022 to 2023
$2.0M
Targeting circulating endothelial glycocalyx fragments to reduce septic encephalopathyR01GM125095 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI HERSON, PACO S, SCHMIDT, ERIC PETER · 2017 to 2020
$1.9M
Mechanisms driving endothelial angiopoietin-2 expression and vascular dysfunction during pediatric sepsisK08GM144788 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RICHTER, ROBERT P · 2021 to 2025
$930k
Eunice Kennedy Shriver National Institute of Child Health and Human Development K12HD047349Eunice Kennedy Shriver National Institute of Child Health and Human Development K23HD096018Eunice Kennedy Shriver National Institute of Child Health and Human Development R01HD092471National Heart and Lung Institute K08HL159353National Heart and Lung Institute R01HL171101NHLBI NIH HHS R01HL125371NIGMS NIH HHS K08 GM144788NIGMS NIH HHS K08GM144788NIGMS NIH HHS R01GM125095NIGMS NIH HHS R44GM142304
6 · The paper itself

Abstract

Endothelial glycocalyx (eGCX) shedding contributes to microvascular endotheliopathy in Acute Respiratory Distress Syndrome (ARDS) and may represent an underrecognized source of phenotypic heterogeneity. We examined whether circulating heparan sulfate (HS) signatures, as readouts of eGCX shedding, capture patterns of inter-patient biological variation distinct from other eGCX components and conventional protein biomarkers, whether specific HS structural features are enriched, and whether these signatures are associated with heparanase-1 (HPSE) activity. We retrospectively analyzed prospectively collected plasma samples (2018-2020) from children with and without pediatric ARDS (PARDS). Plasma levels (ng/mL) of sulfated and non-sulfated HS disaccharides (following enzymatic digestion of total [unfractionated] HS), and HPSE activity (U/mL) were measured using mass spectrometry, while protein biomarkers were assessed by multiplex assay. Among 46 children (36 PARDS, 10 no PARDS), principal component analysis identified three components explaining > 60% of the variance. The primary component (PC1) was characterized by an HS-driven endothelial signature and was distinct from an inflammatory protein signature captured by PC2. In PARDS, children with higher PC1 scores had worse organ dysfunction and fewer ventilator-free days after adjustment for PC2 and PC3. Higher total HS levels were further associated with selective enrichment of sulfated HS motifs, whereas the opposite pattern was observed in non-PARDS. HPSE activity positively correlated with circulating HS levels. These preliminary findings suggest that circulating HS signatures capture a distinct and clinically meaningful dimension of PARDS heterogeneity.

Indexed as

Biological heterogeneityEndothelial glycocalyxHeparanaseHeparan sulfateMass spectrometryPediatric Acute Respiratory Distress Syndrome

Identifiers

PMID42362731

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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.