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논문 기본 정보

자료유형
학술저널
저자정보
Jun-ichi Abe (The University of Texas MD Anderson Cancer Center) Nhat-Tu Le (The University of Texas MD Anderson Cancer Center) 허경선 (The University of Texas MD Anderson Cancer Center)
저널정보
대한의용생체공학회 Biomedical Engineering Letters (BMEL) Biomedical Engineering Letters (BMEL) Vol.5 No.3
발행연도
2015.1
수록면
162 - 171 (10page)

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초록· 키워드

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Although atherosclerosis is a multi-factorial disease, thefocalization of atherosclerotic plaques on the vessel wallsuggests that local factors such as patterns of local bloodflow are critical in the progression of atherosclerosis. Bloodflow creates various types of forces onto the surface ofvascular endothelial cells (ECs). Among those various typesof forces, fluid shear stress has a major influence on thestructure and function of ECs. At the branch points and thelesser curvature of the aortic arch, blood flow is disturbed (dflow)and atherosclerotic plaques are frequently detected. Atthe straight parts of the arterial tree and the greater curvatureof aortic arch, blood flow is steady (s-flow, high shear stress)and atherosclerotic plaques are rare. These two patterns ofblood flow (d-flow and s-flow) affects EC structure andfunction differently. However, molecular mechanisms underlinethe difference remains unclear. To provide insights into thisquestion, studies have suggested a number of theories withmultiple proposed signaling pathways, and the role ofpost-translational modifications has emerged. Particularly,SUMOylation is highlighted based on its potentiality toregulate a wide range of cellular functions. EC dysfunctioninduced by SUMOylation is proposed to accelerate d-flowinducedatherosclerosis. In this review, we focus onSUMOylation and its role in regulating transcriptional networksand propose a mechanistic link between d-flow and ECdysfunction. Since a strong correlation exists between d-flowand atherosclerotic plaque formation, understanding themechanism of d-flow-induced SUMOylation events mayreveal new paths towards therapeutic interventions againstEC dysfunction and atherosclerosis.

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