Evidence map›Paper›PMID 31380363›Full record

ReviewFrontiers in bioengineering and biotechnology2019

Endothelial Cell Mechano-Metabolomic Coupling to Disease States in the Lung Microvasculature.

David Wu, Konstantin Birukov

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in bioengineering and biotechnology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Advancements in preclinical human-relevant modeling of pulmonary vasculature on-chip.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Lung pericytes as mediators of inflammation.American journal of physiology. Lung cellular and molecular physiology · 2023
    Review
  14. Article
  15. Lung Tissue Engineering: Toward a More Deliberate Approach.ACS biomaterials science & engineering · 2022
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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 2 institutions in 1 country.

David WuSection of Pulmonary and Critical Care, Department of Medicine, University of Chicago, Chicago, IL, United States.
Konstantin BirukovDepartment of Anesthesia, University of Maryland, Baltimore, MD, United States.
University of Chicago · USUniversity of Maryland, Baltimore · US

Funding

Control of Lung Permeability by Oxidized PhospholipidsR01HL076259 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2004 to 2023
$6.8M
Molecular control of lung endothelial barrier function in ALIR01HL087823 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2008 to 2020
$4.6M
Modulation of inflammation in aging lungR01HL146829 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2020 to 2023
$1.5M
Phospholipidomics and inflammation in sepsisR01GM122940 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2017 to 2020
$1.2M
Regulation of vascular metabolism in acute lung injuryR00HL145113 · NHLBI · UNIVERSITY OF CHICAGO · PI WU, DAVID D · 2021 to 2022
$341k
Regulation of vascular metabolism in acute lung injuryK99HL145113 · NHLBI · UNIVERSITY OF CHICAGO · PI WU, DAVID D · 2019 to 2020
$320k
NHLBI NIH HHS K99 HL145113NHLBI NIH HHS R00 HL145113NHLBI NIH HHS R01 HL087823NHLBI NIH HHS R01 HL146829NIGMS NIH HHS R01 GM122940
6 · The paper itself

Abstract

Lungs are the most vascular part of humans, accepting the totality of cardiac output in a volume much smaller than the body itself. Due to this cardiac output, the lung microvasculature is subject to mechanical forces including shear stress and cyclic stretch that vary with the cardiac and breathing cycle. Vessels are surrounded by extracellular matrix which dictates the stiffness which endothelial cells also sense and respond to. Shear stress, stiffness, and cyclic stretch are known to influence endothelial cell state. At high shear stress, endothelial cells exhibit cell quiescence marked by low inflammatory markers and high nitric oxide synthesis, whereas at low shear stress, endothelial cells are thought to "activate" into a pro-inflammatory state and have low nitric oxide. Shear stress' profound effect on vascular phenotype is most apparent in the arterial vasculature and in the pathophysiology of vascular inflammation. To conduct the flow of blood from the right heart, the lung microvasculature must be rigid yet compliant. It turns out that excessive substrate rigidity or stiffness is important in the development of pulmonary hypertension and chronic fibrosing lung diseases via excessive cell proliferation or the endothelial-mesenchymal transition. Recently, a new body of literature has evolved that couples mechanical sensing to endothelial phenotypic changes through metabolic signaling in clinically relevant contexts such as pulmonary hypertension, lung injury syndromes, as well as fibrosis, which is the focus of this review. Stretch, like flow, has profound effect on endothelial phenotype; metabolism studies due to stretch are in their infancy.

Indexed as

endothelial (dys)functionendothelial mesenchymal transitionmetabolismmicrovasculaturepulmonary

Identifiers

PMID31380363
PMCPMC6658821
OpenAlexW2956315760

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.