Evidence map›Paper›PMID 32951280›Full record

ReviewJournal of cellular and molecular medicine2020

The role of endothelial shear stress on haemodynamics, inflammation, coagulation and glycocalyx during sepsis.

Florea Lupu, Gary Kinasewitz, Kenneth Dormer

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
8.3field-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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Inflammatory pathways in transfusion-associated circulatory overload.Blood vessels, thrombosis & hemostasis · 2025
    Article
  13. Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Sex differences of sequential changes in coronary blood flow and microvascular function in patients with suspected angina.Clinical research in cardiology : official journal of the German Cardiac Society · 2024
    Article
  18. Article
  19. Review
  20. Article

12 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 1 country.

Florea LupuCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.ORCID 0000-0003-1249-9278
Gary KinasewitzCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Kenneth DormerVasoactiv Biomedical Technologies, Tulsa, OK, USA.
Oklahoma Medical Research Foundation · USUniversity of Tulsa · US

Funding

Translation of immunologic technologies from basic research into pre-clinical nonU19AI062629 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 2004 to 2023
$56.2M
Pilot ProjectP30GM114731 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2016 to 2020
$6.5M
FXI and SepsisR01GM116184 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI LUPU, FLOREA, MCCARTY, OWEN J · 2015 to 2018
$1.9M
Coagulation and Complement Activation in SepsisR01GM121601 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI LUPU, FLOREA · 2017 to 2020
$1.6M
Viral miRs and cellular miRs in sepsisR01GM122775 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CALIN, GEORGE A., LUPU, FLOREA · 2018 to 2020
$1.1M
NIAID NIH HHS U19 AI062629NIAID NIH HHS U19AI062629NIGMS NIH HHS P30 GM114731NIGMS NIH HHS P30GM114731NIGMS NIH HHS R01GM116184NIGMS NIH HHS R01 GM121601NIGMS NIH HHS R01GM121601NIGMS NIH HHS R01GM122775
6 · The paper itself

Abstract

Sepsis is a multifactorial syndrome primarily determined by the host response to an invading pathogen. It is common, with over 48 million cases worldwide in 2017, and often lethal. The sequence of events in sepsis begins with the damage of endothelium within the microvasculature, as a consequence of the inflammatory and coagulopathic responses to the pathogen that can progress to multiple organ failure and death. Most therapeutic interventions target the inflammation and coagulation pathways that act as an auto-amplified vicious cycle, which, if unchecked can be fatal. Normal blood flow and shear stress acting on a healthy endothelium and intact glycocalyx have anti-inflammatory, anticoagulant and self-repairing effects. During early stages of sepsis, the vascular endothelium and its glycocalyx become dysfunctional, yet they are essential components of resuscitation and recovery from sepsis. The effects of shear forces on sepsis-induced endothelial dysfunction, including inflammation, coagulation, complement activation and microcirculatory breakdown are reviewed. It is suggested that early therapeutic strategies should prioritize on the restoration of shear forces and endothelial function and on the preservation of the endothelial-glycocalyx barrier.

Indexed as

HemodynamicsAnimalsBlood CoagulationEndothelium, VascularGlycocalyxHomeostasisHumansInflammationSepsisShear StrengthStress, Mechanicalbarrier functioncoagulopathyglycocalyxhaemodynamicsinflammationmechanotransductionsepsisshear stress

Identifiers

PMID32951280
PMCPMC7687012
OpenAlexW3087533667

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.