Evidence map›Paper›PMID 28187268›Full record

ArticleAmerican journal of respiratory cell and molecular biology2017

Fibroblast Growth Factor Signaling Mediates Pulmonary Endothelial Glycocalyx Reconstitution.

Yimu Yang, Sarah M Haeger, Matthew A Suflita, Fuming Zhang, Kyrie L Dailey, James F Colbert, Joshay A Ford, Mario A Picon, Robert S Stearman, Lei Lin and 4 more

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Airway macrophage specific glycocalyx expression and remodeling following viral infection.Matrix biology : journal of the International Society for Matrix Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Mechanisms of lung crosstalk with end organs: scientific session V-ReSPIRE 2025.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  7. Review
  8. The endothelium at the interface between tissues andClinical microbiology reviews · 2025
    Review
  9. Article
  10. Enzymatic Modulation of the Pulmonary Glycocalyx Enhances Susceptibility toAmerican journal of respiratory cell and molecular biology · 2024
    Article
  11. Review
  12. Observational
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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

14 authors at 4 institutions in 1 country.

Yimu Yang1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Sarah M Haeger1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Matthew A SuflitaDepartments of 2 Biology and.
Fuming Zhang3 Chemistry, Rensselaer Polytechnic Institute, Troy, New York.
Kyrie L Dailey1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
James F Colbert1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Joshay A Ford1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Mario A Picon1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
Robert S Stearman4 Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and.
Lei Lin3 Chemistry, Rensselaer Polytechnic Institute, Troy, New York.
Xinyue Liu3 Chemistry, Rensselaer Polytechnic Institute, Troy, New York.
Xiaorui Han3 Chemistry, Rensselaer Polytechnic Institute, Troy, New York.
Robert J Linhardt3 Chemistry, Rensselaer Polytechnic Institute, Troy, New York.
Eric P Schmidt1 Department of Medicine, University of Colorado Denver, Aurora, Colorado.
University of Colorado Denver · USRensselaer Polytechnic Institute · USDenver Health Medical Center · USIndiana University School of Medicine

Funding

Medical Scientist Training ProgramT32GM008497 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI WILSON, CARA C. · 1993 to 2022
$15.2M
PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM007635 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 1985 to 2023
$6.1M
Endothelial glycocalyx reconstitution during sepsisR01HL125371 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI LINHARDT, ROBERT J, SCHMIDT, ERIC PETER · 2014 to 2018
$3.4M
Aging-related changes in gut microbiome mediate septic kidney injuryR03AG056353 · NIA · UNIVERSITY OF COLORADO DENVER · PI COLBERT, JAMES F · 2017 to 2018
$233k
NHLBI NIH HHS R01 HL125371NIA NIH HHS R03 AG056353NIGMS NIH HHS T32 GM007635NIGMS NIH HHS T32 GM008497
6 · The paper itself

Abstract

The endothelial glycocalyx is a heparan sulfate (HS)-rich endovascular structure critical to endothelial function. Accordingly, endothelial glycocalyx degradation during sepsis contributes to tissue edema and organ injury. We determined the endogenous mechanisms governing pulmonary endothelial glycocalyx reconstitution, and if these reparative mechanisms are impaired during sepsis. We performed intravital microscopy of wild-type and transgenic mice to determine the rapidity of pulmonary endothelial glycocalyx reconstitution after nonseptic (heparinase-III mediated) or septic (cecal ligation and puncture mediated) endothelial glycocalyx degradation. We used mass spectrometry, surface plasmon resonance, and in vitro studies of human and mouse samples to determine the structure of HS fragments released during glycocalyx degradation and their impact on fibroblast growth factor receptor (FGFR) 1 signaling, a mediator of endothelial repair. Homeostatic pulmonary endothelial glycocalyx reconstitution occurred rapidly after nonseptic degradation and was associated with induction of the HS biosynthetic enzyme, exostosin (EXT)-1. In contrast, sepsis was characterized by loss of pulmonary EXT1 expression and delayed glycocalyx reconstitution. Rapid glycocalyx recovery after nonseptic degradation was dependent upon induction of FGFR1 expression and was augmented by FGF-promoting effects of circulating HS fragments released during glycocalyx degradation. Although sepsis-released HS fragments maintained this ability to activate FGFR1, sepsis was associated with the downstream absence of reparative pulmonary endothelial FGFR1 induction. Sepsis may cause vascular injury not only via glycocalyx degradation, but also by impairing FGFR1/EXT1-mediated glycocalyx reconstitution.

Indexed as

Signal TransductionAnimalsCecumEndothelium, VascularExostosin 1Fibroblast Growth Factor 2GlycocalyxHeparan SulfateHomeostasisLigationLungMaleMice, Inbred C57BLN-AcetylglucosaminyltransferasesPolysaccharide-LyasesPuncturesExostosin 1Fibroblast Growth Factor 2Heparan Sulfateheparitinsulfate lyaseN-AcetylglucosaminyltransferasesPolysaccharide-LyasesReceptor, Fibroblast Growth Factor, Type 1fibroblast growth factorheparan sulfatesepsis

Identifiers

PMID28187268
PMCPMC5516293
OpenAlexW2586582116

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.