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Cited by 2,280Cellular Mechanics and InteractionsAtherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin Effects

Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives

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Chiu, Jeng-Jiann, Chien, Shu·2011·Physiological Reviews
DOI 10.1152/physrev.00047.2009PMC PMC3844671
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Abstract

Vascular endothelial cells (ECs) are exposed to hemodynamic forces, which modulate EC functions and vascular biology/pathobiology in health and disease. The flow patterns and hemodynamic forces are not uniform in the vascular system. In straight parts of the arterial tree, blood flow is generally laminar and wall shear stress is high and directed; in branches and curvatures, blood flow is disturbed with nonuniform and irregular distribution of low wall shear stress. Sustained laminar flow with high shear stress upregulates expressions of EC genes and proteins that are protective against atherosclerosis, whereas disturbed flow with associated reciprocating, low shear stress generally upregulates the EC genes and proteins that promote atherogenesis. These findings have led to the concept that the disturbed flow pattern in branch points and curvatures causes the preferential localization of atherosclerotic lesions. Disturbed flow also results in postsurgical neointimal hyperplasia and contributes to pathophysiology of clinical conditions such as in-stent restenosis, vein bypass graft failure, and transplant vasculopathy, as well as aortic valve calcification. In the venous system, disturbed flow resulting from reflux, outflow obstruction, and/or stasis leads to venous inflammation and thrombosis, and hence the development of chronic venous diseases. Understanding of the effects of disturbed flow on ECs can provide mechanistic insights into the role of complex flow patterns in pathogenesis of vascular diseases and can help to elucidate the phenotypic and functional differences between quiescent (nonatherogenic/nonthrombogenic) and activated (atherogenic/thrombogenic) ECs. This review summarizes the current knowledge on the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications. Such information can contribute to our understanding of the etiology of lesion development in vascular niches with disturbed flow and help to generate new approaches for therapeutic interventions.

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  • Repeated high-intensity exercise may alter hemodynamics by increasing shear stress, particularly in proximal coronary segments, potentially promoting focal atherosclerosis.

    “First, repeated high-intensity exercise may alter hemodynamics by increasing shear stress, particularly in proximal coronary segments, potentially promoting focal atherosclerosis.12,29,30”

    From Wearable-Derived Training Load and Coronary Atherosclerosis in Middle-Aged and Older Athletes and Physically Active Controls: A New Perspective From the Master@Heart Study (2026) · cites this paper as [30]

    Section VIII.A (page unavailable) agrees that exercise increases flow and shear stress, but says this may retard or reverse coronary artery disease—not promote it. Section V.B (page unavailable) reports lesions in low-shear regions and none in a high-shear region. The cited passages do not identify proximal coronary segments as a site of exercise-related focal atherosclerosis. (LLM, conf=0.88)

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Authors
Chiu, J.-J., & Chien, S.
Affiliations
National Health Research Institutes (TW)
Corresponding author
Chien, Shu
ORCID
Venue
Physiological Reviews
Publisher
American Physiological Society
Published
2011-01
Volume
91
Issue
1
Pages
327-387
ISSN
  • 0031-9333 (ISSN-L)
  • 1522-1210
DOI
10.1152/physrev.00047.2009
PMC
PMC3844671
OpenAlex
W2115533377
Cited by
2,280
References
12
Citations by year
2026: 189 · 2025: 200 · 2024: 181 · 2023: 165 · 2022: 157 · 2021: 196 · 2020: 159 · 2019: 137 · 2018: 146 · 2017: 144 · 2016: 137 · 2015: 121 · 2014: 132 · 2013: 124 · 2012: 65
FWCI
9.46
Type
journal article
Language
en
Open access
Locations
  • Physiological Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL106579, HL104402, HL106579, R21HL104402)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
flow disturbance, vascular endothelium, wall shear stress, atherogenesis, atherosclerosis, hemodynamics, endothelial activation, intimal hyperplasia, in-stent restenosis, vein graft failure, transplant vasculopathy, aortic valve calcification, venous thrombosis, chronic venous disease, endothelial gene expression
MeSH terms
Animals, Endothelium, Vascular, Heart Valve Diseases, Humans, Stress, Mechanical, Vascular Diseases, Hemorheology, Endothelial Cells

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