Evidence map›Paper›PMID 24876354›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2014

Shear stress-initiated signaling and its regulation of endothelial function.

Jing Zhou, Yi-Shuan Li, Shu Chien

Open access · greenAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 338 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
338citing papers in PubMed, 2 pooled it
12.0field-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.

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

338 citing papers in PubMed, 2 syntheses or guidelines pooled it, 539 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
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  5. Review
  6. Article
  7. A Vein Attempt? Experimental Models for Arteriovenous Fistula Research.Cardiovascular engineering and technology · 2026
    Review
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  14. Aging and DNA damage are associated with the development of endothelial cell clonal expansion.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  15. Review
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278 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 1 institution in 1 country.

Jing ZhouFrom the Department of Physiology and Pathophysiology, Basic Medical College of Peking University, Peking University, Beijing, People's Republic of China (J.Z.); and Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (J.Z., Y.-S.L., S.C.). zhoujing1723@gmail.com shuchien@ucsd.edu.
Yi-Shuan LiFrom the Department of Physiology and Pathophysiology, Basic Medical College of Peking University, Peking University, Beijing, People's Republic of China (J.Z.); and Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (J.Z., Y.-S.L., S.C.).
Shu ChienFrom the Department of Physiology and Pathophysiology, Basic Medical College of Peking University, Peking University, Beijing, People's Republic of China (J.Z.); and Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (J.Z., Y.-S.L., S.C.). zhoujing1723@gmail.com shuchien@ucsd.edu.
Peking University · CN

Funding

Systems Biology Analyses for Hemodynamic Regulation of Vascular HomeostasisR01HL108735 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2012 to 2024
$13.4M
Shear Regulation of MicroRNA Transportomes and Targetomes in Vascular HomeostasisR01HL106579 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2011 to 2022
$8.3M
Role of Spatiotemporal Epigenetic Dynamics in Regulating Endothelial Gene Expressions under FlowsR01HL121365 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHIEN, SHU, WANG, YINGXIAO · 2014 to 2025
$7.5M
NHLBI NIH HHS HL106579NHLBI NIH HHS HL108735NHLBI NIH HHS HL121365NHLBI NIH HHS R01 HL106579NHLBI NIH HHS R01 HL108735NHLBI NIH HHS R01 HL121365
6 · The paper itself

Abstract

Atherosclerosis develops preferentially at branches and curvatures of the arterial tree, where blood flow pattern is disturbed rather than being laminar, and wall shear stress has an irregular distribution without defined directions. The endothelium in the atherosusceptible regions, in comparison to that in atheroresistant regions, shows activation of proproliferative and proinflammatory gene expressions, reduced production of nitric oxide (NO), increased leukocyte adhesion, and permeability, as well as other atheroprone phenotypes. Differences in gene expressions and cell phenotypes have been detected in endothelia residing in native atherosusceptible and atheroresistant regions of the arteries, or in arteries from animal models with artificial creation of disturbed flow. Similar results have also been shown in in vitro systems that apply controlled shear stresses with or without clear directions to cultured endothelial cells in fluid-dynamically designed flow-loading devices. The available evidence indicates that the coordination of multiple signaling networks, rather than individual separate pathways, links the mechanical signals to specific genetic circuitries in orchestrating the mechanoresponsive networks to evoke comprehensive genetic and functional responses.

Indexed as

Mechanotransduction, CellularAnimalsAtherosclerosisEndothelial CellsEndothelium, VascularGene Expression RegulationHemodynamicsHumansPhenotypeRegional Blood FlowStress, Mechanicalatherosclerosiscellular mechanotransductionhemodynamics

Identifiers

PMID24876354
PMCPMC4169328
OpenAlexW2074249358

What OpenQuestion holds

Textmetadata
LicenceTDM
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.