Evidence map›Paper›PMID 9598824›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology1998

Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force.

O Traub, B C Berk

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03829046 (The Effects of Evolocumab on Endothelial and Inflammatory Biocellular Markers in Patients With Diabetes and Atherosclerotic Vascular Disease), which is not on this map. Cited by 300 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
300citing papers in PubMed, 3 pooled it
10.8field-weighted citation impact, top 1% 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.

NCT03829046 phase4completedstarted 2019, after this paper: background citation

The Effects of Evolocumab on Endothelial and Inflammatory Biocellular Markers in Patients With Diabetes and Atherosclerotic Vascular Disease (METCHNIKOFF)

Ran2019Enrolled41Registered outcomes11Posted comparisons0ConditionsAtherosclerotic Vascular Disease, Microvascular Dysfunction, Type2 DiabetesArmsEvolocumab, Placebo
Open the trial in the graph
3 · Its place in the literature

Who cites it

300 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,075 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
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  8. Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  9. Hemodynamic Metrics and Arterial Dysfunction: Insights From a Novel Microfluidic Device.International journal for numerical methods in biomedical engineering · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Biology, Physics, and Genetics of Intracranial Aneurysm Formation: A Review.Journal of neurological surgery. Part A, Central European neurosurgery · 2026
    Review
  14. Article
  15. A One-Dimensional (1D) Computational Fluid Dynamics Study of Fontan-Associated Liver Disease (FALD).International journal for numerical methods in biomedical engineering · 2026
    Article
  16. Review
  17. Hemodynamics in carotid artery stenosis.International angiology : a journal of the International Union of Angiology · 2025
    Review
  18. Review
  19. Review
  20. Article

240 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

2 authors at 1 institution in 1 country.

O TraubDepartment of Pathology, The University of Washington, Seattle 98195, USA.
B C Berk
University of Washington · US

Funding

VLA-4 and VCAM-1 in Advanced AtherosclerosisP01HL018645 · NHLBI · UNIVERSITY OF WASHINGTON · PI CHAIT, ALAN · 1985 to 2010
$23.9M
NHLBI NIH HHS P01HL18645NIGMS NIH HHS NIGM-GM07266
6 · The paper itself

Abstract

Mechanical forces are important modulators of cellular function in many tissues and are particularly important in the cardiovascular system. The endothelium, by virtue of its unique location in the vessel wall, responds rapidly and sensitively to the mechanical conditions created by blood flow and the cardiac cycle. In this study, we examine data which suggest that steady laminar shear stress stimulates cellular responses that are essential for endothelial cell function and are atheroprotective. We explore the ability of shear stress to modulate atherogenesis via its effects on endothelial-mediated alterations in coagulation, leukocyte and monocyte migration, smooth muscle growth, lipoprotein uptake and metabolism, and endothelial cell survival. We also propose a model of signal transduction for the endothelial cell response to shear stress including possible mechanotransducers (integrins, caveolae, ion channels, and G proteins), intermediate signaling molecules (c-Src, ras, Raf, protein kinase C) and the mitogen activated protein kinases (ERK1/2, JNK, p38, BMK-1), and effector molecules (nitric oxide). The endothelial cell response to shear stress may also provide a mechanism by which risk factors such as hypertension, diabetes, hypercholesterolemia, and sedentary lifestyle act to promote atherosclerosis.

Indexed as

Mitogen-Activated Protein KinasesSignal TransductionAnimalsArteriosclerosisCalcium-Calmodulin-Dependent Protein KinasesEndothelium, VascularEnzyme ActivationHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MitogensNitric OxideProtein KinasesStress, MechanicalCalcium-Calmodulin-Dependent Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesMitogensNitric OxideProtein Kinases

Identifiers

PMID9598824
OpenAlexW2147367812

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.