Investigation of Wall Shear Stress in Cardiovascular Research and in Clinical Practice—From Bench to Bedside

In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyp...

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Vydané v:International journal of molecular sciences Ročník 22; číslo 11; s. 5635
Hlavní autori: Urschel, Katharina, Tauchi, Miyuki, Achenbach, Stephan, Dietel, Barbara
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Switzerland MDPI 26.05.2021
Predmet:
Coronary Artery Disease - metabolism
Coronary Artery Disease - pathology
Coronary Artery Disease - physiopathology
Coronary Circulation
Endothelial Cells - metabolism
Endothelial Cells - pathology
Humans
Plaque, Atherosclerotic - metabolism
Plaque, Atherosclerotic - pathology
Plaque, Atherosclerotic - physiopathology
Plaque, Atherosclerotic - therapy
Review
Shear Strength
Stress, Mechanical
atherosclerosis
glycocalyx
plaque
mechanotransduction
wall shear stress
endothelial activation
rupture
ISSN:1422-0067, 1422-0067
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Abstract In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as “wall shear stress (WSS)”, and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.
AbstractList In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as "wall shear stress (WSS)", and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as "wall shear stress (WSS)", and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.
In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as “wall shear stress (WSS)”, and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.
Author Tauchi, Miyuki
Achenbach, Stephan
Urschel, Katharina
Dietel, Barbara
AuthorAffiliation Department of Medicine 2—Cardiology and Angiology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Universitätsklinikum, 91054 Erlangen, Germany; Katharina.Urschel@uk-erlangen.de (K.U.); miyuki.tauchi@uk-erlangen.de (M.T.); Stephan.Achenbach@uk-erlangen.de (S.A.)
AuthorAffiliation_xml – name: Department of Medicine 2—Cardiology and Angiology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Universitätsklinikum, 91054 Erlangen, Germany; Katharina.Urschel@uk-erlangen.de (K.U.); miyuki.tauchi@uk-erlangen.de (M.T.); Stephan.Achenbach@uk-erlangen.de (S.A.)
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  surname: Urschel
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  fullname: Dietel, Barbara
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Issue 11
Keywords atherosclerosis
glycocalyx
plaque
mechanotransduction
wall shear stress
endothelial activation
rupture
Language English
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Snippet In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted...
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StartPage 5635
SubjectTerms Coronary Artery Disease - metabolism
Coronary Artery Disease - pathology
Coronary Artery Disease - physiopathology
Coronary Circulation
Endothelial Cells - metabolism
Endothelial Cells - pathology
Humans
Plaque, Atherosclerotic - metabolism
Plaque, Atherosclerotic - pathology
Plaque, Atherosclerotic - physiopathology
Plaque, Atherosclerotic - therapy
Review
Shear Strength
Stress, Mechanical
Title Investigation of Wall Shear Stress in Cardiovascular Research and in Clinical Practice—From Bench to Bedside
URI https://www.ncbi.nlm.nih.gov/pubmed/34073212
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https://pubmed.ncbi.nlm.nih.gov/PMC8198948
Volume 22
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