Abstract
Although atherosclerosis is a multi-factorial disease, the focalization of atherosclerotic plaques on the vessel wall suggests that local factors such as patterns of local blood flow are critical in the progression of atherosclerosis. Blood flow creates various types of forces onto the surface of vascular endothelial cells (ECs). Among those various types of forces, fluid shear stress has a major influence on the structure and function of ECs. At the branch points and the lesser curvature of the aortic arch, blood flow is disturbed (dflow) and atherosclerotic plaques are frequently detected. At the straight parts of the arterial tree and the greater curvature of aortic arch, blood flow is steady (s-flow, high shear stress) and atherosclerotic plaques are rare. These two patterns of blood flow (d-flow and s-flow) affects EC structure and function differently. However, molecular mechanisms underline the difference remains unclear. To provide insights into this question, studies have suggested a number of theories with multiple proposed signaling pathways, and the role of post-translational modifications has emerged. Particularly, SUMOylation is highlighted based on its potentiality to regulate a wide range of cellular functions. EC dysfunction induced by SUMOylation is proposed to accelerate d-flowinduced atherosclerosis. In this review, we focus on SUMOylation and its role in regulating transcriptional networks and propose a mechanistic link between d-flow and EC dysfunction. Since a strong correlation exists between d-flow and atherosclerotic plaque formation, understanding the mechanism of d-flow-induced SUMOylation events may reveal new paths towards therapeutic interventions against EC dysfunction and atherosclerosis.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 162-171 |
| Number of pages | 10 |
| Journal | Biomedical Engineering Letters |
| Volume | 5 |
| Issue number | 3 |
| DOIs | |
| State | Published - Sep 1 2015 |
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Keywords
- Atherosclerosis
- Disturbed flow
- EC dysfunction
- SUMOylation
- Steady flow
ASJC Scopus subject areas
- Biomedical Engineering
Cite this
Role for SUMOylation in disturbed flow-induced atherosclerotic plaque formation. / Abe, Jun ichi; Le, Nhat Tu; Heo, Kyung Sun.
In: Biomedical Engineering Letters, Vol. 5, No. 3, 01.09.2015, p. 162-171.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Role for SUMOylation in disturbed flow-induced atherosclerotic plaque formation
AU - Abe, Jun ichi
AU - Le, Nhat Tu
AU - Heo, Kyung Sun
PY - 2015/9/1
Y1 - 2015/9/1
N2 - Although atherosclerosis is a multi-factorial disease, the focalization of atherosclerotic plaques on the vessel wall suggests that local factors such as patterns of local blood flow are critical in the progression of atherosclerosis. Blood flow creates various types of forces onto the surface of vascular endothelial cells (ECs). Among those various types of forces, fluid shear stress has a major influence on the structure and function of ECs. At the branch points and the lesser curvature of the aortic arch, blood flow is disturbed (dflow) and atherosclerotic plaques are frequently detected. At the straight parts of the arterial tree and the greater curvature of aortic arch, blood flow is steady (s-flow, high shear stress) and atherosclerotic plaques are rare. These two patterns of blood flow (d-flow and s-flow) affects EC structure and function differently. However, molecular mechanisms underline the difference remains unclear. To provide insights into this question, studies have suggested a number of theories with multiple proposed signaling pathways, and the role of post-translational modifications has emerged. Particularly, SUMOylation is highlighted based on its potentiality to regulate a wide range of cellular functions. EC dysfunction induced by SUMOylation is proposed to accelerate d-flowinduced atherosclerosis. In this review, we focus on SUMOylation and its role in regulating transcriptional networks and propose a mechanistic link between d-flow and EC dysfunction. Since a strong correlation exists between d-flow and atherosclerotic plaque formation, understanding the mechanism of d-flow-induced SUMOylation events may reveal new paths towards therapeutic interventions against EC dysfunction and atherosclerosis.
AB - Although atherosclerosis is a multi-factorial disease, the focalization of atherosclerotic plaques on the vessel wall suggests that local factors such as patterns of local blood flow are critical in the progression of atherosclerosis. Blood flow creates various types of forces onto the surface of vascular endothelial cells (ECs). Among those various types of forces, fluid shear stress has a major influence on the structure and function of ECs. At the branch points and the lesser curvature of the aortic arch, blood flow is disturbed (dflow) and atherosclerotic plaques are frequently detected. At the straight parts of the arterial tree and the greater curvature of aortic arch, blood flow is steady (s-flow, high shear stress) and atherosclerotic plaques are rare. These two patterns of blood flow (d-flow and s-flow) affects EC structure and function differently. However, molecular mechanisms underline the difference remains unclear. To provide insights into this question, studies have suggested a number of theories with multiple proposed signaling pathways, and the role of post-translational modifications has emerged. Particularly, SUMOylation is highlighted based on its potentiality to regulate a wide range of cellular functions. EC dysfunction induced by SUMOylation is proposed to accelerate d-flowinduced atherosclerosis. In this review, we focus on SUMOylation and its role in regulating transcriptional networks and propose a mechanistic link between d-flow and EC dysfunction. Since a strong correlation exists between d-flow and atherosclerotic plaque formation, understanding the mechanism of d-flow-induced SUMOylation events may reveal new paths towards therapeutic interventions against EC dysfunction and atherosclerosis.
KW - Atherosclerosis
KW - Disturbed flow
KW - EC dysfunction
KW - SUMOylation
KW - Steady flow
UR - http://www.scopus.com/inward/record.url?scp=84944457229&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84944457229&partnerID=8YFLogxK
U2 - 10.1007/s13534-015-0199-6
DO - 10.1007/s13534-015-0199-6
M3 - Review article
AN - SCOPUS:84944457229
VL - 5
SP - 162
EP - 171
JO - Biomedical Engineering Letters
JF - Biomedical Engineering Letters
SN - 2093-9868
IS - 3
ER -