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Updated: Aug 22, 2026

In Vitro Model of Physiological and Pathological Blood Flow with Application to Investigations of Vascular Cell Remodeling
Published on: November 3, 2015
Molecular and biological effects of hemodynamics on vascular cells
Sanjeev Pradhan1, Bauer Sumpio
1Department of Surgery, Yale University School of Medicine and VA Connecticut, USA.
Insights
Cyclic strain, a force on vessel walls, influences endothelial cells to resist atherosclerosis. This review details how mechanical forces impact vascular biology and plaque development.
Area of Science:
- Cardiovascular Biology
- Biomedical Engineering
- Vascular Cell Biology
Background:
- Systemic risk factors like smoking, hypertension, hyperlipidemia, and diabetes promote atherosclerosis.
- Clinically significant atherosclerotic lesions often develop at specific vascular locations, such as branch points and bifurcations.
- This suggests a complex interaction between vascular anatomy, biology, and hemodynamic forces in plaque development.
Purpose of the Study:
- To review the current literature on the effects of cyclic strain on endothelial cells.
- To summarize how mechanical forces influence vascular biology in the context of atherosclerosis.
Main Methods:
- Literature review of studies investigating cyclic strain and endothelial cell responses.
- Analysis of research on molecular and cellular changes induced by cyclic strain.
Main Results:
- Cyclic strain induces endothelial cell migration, proliferation, and cytoskeletal changes that may inhibit atherosclerosis.
- Mechanical forces alter the production of key macromolecules like nitric oxide and endothelin.
- Cyclic strain modulates the expression of cellular adhesion molecules (e.g., ICAM-1) and intracellular signaling pathways (e.g., cAMP, protein kinase C).
Conclusions:
- Cyclic strain is a significant hemodynamic factor influencing endothelial cell behavior.
- Understanding these effects is crucial for elucidating the mechanisms underlying atherosclerosis development at specific arterial sites.
Abstract:
A variety of systemic risk factors, including smoking, hypertension, hyperlipidemia and diabetes have been found to promote atherosclerosis. Although these elements affect blood vessels equally, clinically significant lesions develop at predictable locations, i.e., major branch points and bifurcations. This suggests that the development of clinically significant atherosclerotic plaques involves a complex interplay between vascular anatomy, vascular biology and hemodynamic forces. Cyclic strain, circumferential pulsatile pressure exerted upon a vessel wall, has been found to cause changes in endothelial cells that tend to disfavor atherosclerosis formation. Cultured endothelial cells have been shown to migrate, proliferate and alter cytoskeletal alignment in response to cyclic strain. Levels of macromolecules such as prostacyclin, endothelin, nitric oxide and tissue plasminogen activator have been found to be altered by cyclic strain. Additionally, cyclic strain has been shown to stimulate expression of cellular adhesion molecules such as ICAM-1 and intracellular second messenger systems such as the adenylate cyclase-cAMP, diacylglycerol-IP3, and protein kinase C pathways. This article reviews the most current pertinent literature and summarizes the presently known effects of cyclic strain on endothelial cells.
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