• Title, Summary, Keyword: atherosclerosis

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A Comparative Study of the Hemodynamic Hypotheses for the Generation of Atherosclerosis (동맥경화증의 발생에 관한 혈류역학적 가설들에 대한 비교연구)

  • Suh, Sang-Ho;Cho, Min-Tae;Roh, Hyung-Woon;Kwon, Hyuck-Moon
    • Proceedings of the KSME Conference
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    • pp.1915-1918
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    • 2003
  • Atherosclerosis, which is a degenerate disease, is believed to occur in the vascular system due to deposition of cholesterol and low density lipoprotein(LDL) or thrombosis on the blood vessel. Atherosclerosis narrows arterial lumen, which is known as stenosis phenomenon of blood vessel. Pathogenesis of atherosclerosis is thought to occur mainly by aging. Restenosis phenomenon is observed in the same site of insertion of a stent and balloon angioplasty after treatment of interventional theraphy. Several hypothetical theories related to the generation of atherosclerosis have been reported: high shear stress theory, low shear stress theory, high shear stress gradient theory, flow separation and turbulence theory and high pressure theory. However, no one theory clearly explains the causes of atherosclerosis. In the present study the generation of atherosclerosis in the left coronary artery is investigated. The hypotheses are verified by using the computer simulation.

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Contrasting Roles of Different Endoglin Forms in Atherosclerosis

  • Jang, Young-Saeng;Choi, In-Hong
    • IMMUNE NETWORK
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    • v.14 no.5
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    • pp.237-240
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    • 2014
  • Endoglin (also known as CD105 or TGF-${\beta}$ type III receptor) is a co-receptor involved in TGF-${\beta}$ signaling. In atherosclerosis, TGF-${\beta}$ signaling is crucial in regulating disease progression owing to its anti-inflammatory effects as well as its inhibitory effects on smooth muscle cell proliferation and migration. Endoglin is a regulator of TGF-${\beta}$ signaling, but its role in atherosclerosis has yet to be defined. This review focuses on the roles of the various forms of endoglin in atherosclerosis. The expression of the two isoforms of endoglin (long-form and short-form) is increased in atherosclerotic lesions, and the expression of the soluble forms of endoglin is upregulated in sera of patients with hypercholesterolemia and atherosclerosis. Interestingly, long-form endoglin shows an atheroprotective effect via the induction of eNOS expression, while short-form and soluble endoglin enhance atherogenesis by inhibiting eNOS expression and TGF-${\beta}$ signaling. This review summarizes evidence suggesting that the different forms of endoglin have distinct roles in atherosclerosis.

Low Density Lipoprotein(LDL), Atherosclerosis and Antioxidants

  • Ryu, Beung-Ho
    • Biotechnology and Bioprocess Engineering:BBE
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    • v.5 no.5
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    • pp.313-319
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    • 2000
  • A crucial and causative role in the pathogenesis of atherosclerosis is believed to be the oxidative modification of low density lipoprotein (LDL). The oxidation of LDL involves released free radical driven lipid peroxidation. Several lines of evidence support the role of oxidized LDL in atherogenesis. Epidemiologic studies have demonstrated an association between an increased intake of dietary antioxidant vitamins, such as vitamin E and vitamin C and reduced morbidity and mortality from coronary artery diseases. It is thus hypothesized that dietary antioxidants may help prevent the development and progression of atherosclerosis. The oxidation of LDL has been shown to be reduced by antioxidants, and, in animal models, improved antioxidants may offer possibilities for the prevention of atherosclerosis. The results of several on going long randomized intervention trials will provide valuahle information on the efficacy and safety of improved antioxidants in the prevention of atherosclerosis. This review a evaluates current literature involving antioxidants and vascular disease, with a particular focus on the potential mechanisms.

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Role of Interleukin-4 in Atherosclerosis

  • Lee, Yong-Woo;Hirani, Anjali A.
    • Archives of Pharmacal Research
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    • v.29 no.1
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    • pp.1-15
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    • 2006
  • Vascular endothelial cell injury or dysfunction has been implicated in the onset and' progression of cardiovascular diseases including atherosclerosis. A number of previous studies have demonstrated that the pro-oxidative and pro-inflammatory pathways within vascular endothelium play an important role in the initiation and progression of atherosclerosis, Recent evidence has provided compelling evidence to indicate that interleukin-4 (IL-4) can induce proc inflammatory environment via oxidative stress-mediated up-regulation of inflammatory mediators such as cytokine, chemokine, and adhesion molecules in vascular endothelial cells. In addition, apoptotic cell death within vascular endothelium has been hypothesized to be involved in the development of atherosclerosis. Emerging evidence has demonstrated that IL-4 can induce apoptosis of human vascular endothelial cells through the caspase-3-dependent pathway, suggesting that IL-4 can increase endothelial cell turnover by accelerated apoptosis, the event which may cause the dysfunction of the vascular endothelium. These studies will have a high probability of revealing new directions that lead to the development of clinical strategies toward the prevention and/or treatment for individuals with inflammatory vascular diseases including atherosclerosis.

The role of peroxidases in the pathogenesis of atherosclerosis

  • Park, Jong-Gil;Oh, Goo-Taeg
    • BMB Reports
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    • v.44 no.8
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    • pp.497-505
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    • 2011
  • Reactive oxygen species (ROS), which include superoxide anions and peroxides, induce oxidative stress, contributing to the initiation and progression of cardiovascular diseases involving atherosclerosis. The endogenous and exogenous factors hypercholesterolemia, hyperglycemia, hypertension, and shear stress induce various enzyme systems such as nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, and lipoxygenase in vascular and immune cells, which generate ROS. Besides inducing oxidative stress, ROS mediate signaling pathways involved in monocyte adhesion and infiltration, platelet activation, and smooth muscle cell migration. A number of antioxidant enzymes (e.g., superoxide dismutases, catalase, glutathione peroxidases, and peroxiredoxins) regulate ROS in vascular and immune cells. Atherosclerosis results from a local imbalance between ROS production and these antioxidant enzymes. In this review, we will discuss 1) oxidative stress and atherosclerosis, 2) ROS-dependent atherogenic signaling in endothelial cells, macrophages, and vascular smooth muscle cells, 3) roles of peroxidases in atherosclerosis, and 4) antioxidant drugs and therapeutic perspectives.

Visualization on the Functional Changes of Endothelial Cells Due to Apoptotic Macrophage in Atherosclerosis Microenvironment (동맥경화의 미세환경에서 대식세포의 사멸에 의한 혈관세포의 기능적 변화에 대한 가시화)

  • Kim, Wanho;Son, Jegoo;Jeon, Jessie Sungyun
    • Journal of the Korean Society of Visualization
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    • v.15 no.3
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    • pp.41-46
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    • 2017
  • The apoptosis of macrophages occurs throughout all stages of atherosclerosis. It is known to constitute atheromatous plaque, increase plaque instability, and thus contribute to the development of atherosclerosis. However, there still remains much to be elucidated on how the apoptotic macrophages affect the endothelial cells and also how they contribute to the development of atherosclerosis. Here we present a microfluidic system, which enables co-culture of apoptotic macrophages and endothelial cells in fibrin gel that mimics in vivo extracellular matrix. With the system, we can investigate the effect of macrophage apoptosis on vascular endothelial cells by quantitatively analyzing the level of reactive oxygen species of HUVECs, integrity of VE-cadherin and cell proliferation. We expect that this system could be utilized further for understanding different mechanisms of apoptotic macrophage on the development of atherosclerosis.