• 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.

• Biomedical Science Letters
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• v.8 no.4
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• pp.257-268
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• 2002

Chronic infection and inflammation have recently been implicated as important etiologic agents of atherosclerosis. Several agents have been suggested as possible candidates including cytomegalovirus (CMV), herpes simplex vims type 1 (HSV-1), Epstein-Barr virus (EBV), Chlamydia pneumoniae, and Helicobacter pylori. We evaluated the relationship between cytornegalovirus infection and atherosclerosis by in situ hybridization and polymerase chain reaction (PCR). We examined 23 subjects with atherosclerosis and 10 matched control subjects without atherosclerosis. CMV was detected by in situ hybridization in 60.9% (14/23) of aorta and 42.9% (9/21) of coronary arteries in subjects with atherosclerosis. It was also detected by PCR in 65.2% (15/23) of aorta and 52.4% (11/21) of coronary arteries. CMV was detected on areas showing early or advanced atheromatous changes. Cells morphologically identical to smooth muscle cells, endothelial cells, lymphocytes, fibroblasts, and Schwann cells were positively reacted with the CMV probe. However. none of the cells to which the probe hybridized contained inclusion bodies, thus strongly suggesting that the arterial wall may be a site of CMV latency. This result Indicates that CMV may potentially play a direct or indirect role in the pathogenesis of human atherosclerosis.

• 한국약용작물학회:학술대회논문집
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• 2008.05a
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• pp.164-165
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• 2008

• Biomolecules & Therapeutics
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• v.27 no.3
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• pp.254-264
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• 2019

Atherosclerosis is a widespread and chronic progressive arterial disease that has been regarded as one of the major causes of death worldwide. It is caused by the deposition of cholesterol, fats, and other substances in the tunica intima which leads to narrowing of the blood vessels, loss of elasticity, and arterial wall thickening, thus causing difficulty in blood flow. Natural products have been used as one of the most important strategies for the treatment and prevention of cardiovascular diseases for a long time. In recent decades, as interests in natural products including medicinal herbs have increased, many studies regarding natural compounds that are effective against atherosclerosis have been conducted. The purpose of this review is to provide a brief overview of the natural compounds that have been used for the treatment and prevention of atherosclerosis, and their mechanisms of action based on recent research.

• Journal of Chest Surgery
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• v.52 no.2
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• pp.112-115
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• 2019

We describe aortic arch endarterectomy performed concomitantly with on-pump cardiac surgery in 2 patients with grade V arch atherosclerosis. In both patients, transesophageal echocardiographic findings led to the diagnosis of severe arch atherosclerosis associated with a mobile atheromatous plaque in the aortic arch. The severe arch atherosclerosis was managed with endarterectomy under deep hypothermic circulatory arrest. In patients with severe grade V atherosclerosis in the aortic arch, performing endarterectomy simultaneously with primary cardiac surgery may be justified as a way to reduce the risk of peripheral embolism, including cerebrovascular accidents, with minimal additional surgical risk.

• 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.

• Journal of Periodontal and Implant Science
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• v.35 no.1
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• pp.1-8
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• 2005

Bacterial heat shock protein has been one of the components that are responsible to induce autoimmune disease mechanisms in the pathogenesis of atherosclerosis due to high level of homology in sequence with human counterpart. This mechanism may explain how bacterial infectious disease, such as periodontal disease, might contribute to the acceleration of the disease process of atherosclerosis. Porphyromonas gingivalis which is a major periodontal pathogenic bacterial species, has been implicated as one of the pathogenic bacteria playing the role in this context. The present study has been performed to evaluate the anti-atherosclerotic effect of adoptive transfer of Porphyromonas gingivalis heat shock protein epitope-specific T cell lines into severe combined immunodeficiency (SCID) mice. Peptide no. 15 with amino acid sequence VKEVASKTND-specific T cell line was selected for the transfer. When experimental atherosclerosis was induced in SCID mice adoptively transferred either by the T cell lines (experimental group) or by non-specific mouse T cells (control group), there was no significant difference in the severity and extent of the atherosclerosis induced by hypercholesterol diet.

• 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.

• Journal of Ginseng Research
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• v.45 no.1
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• pp.22-31
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• 2021

Atherosclerosis (AS) is a leading cause of cardiovascular diseases (CVDs) and it results in a high rate of death worldwide, with an increased prevalence with age despite advances in lifestyle management and drug therapy. Atherosclerosis is a chronic progressive inflammatory process, and it mainly presents with lipid accumulation, foam cell proliferation, inflammatory response, atherosclerotic plaque formation and rupture, thrombosis, and vascular calcification. Therefore, there is a great need for reliable therapeutic drugs or remedies to cure or alleviate atherosclerosis and reduce the societal burden. Ginsenosides are natural steroid glycosides and triterpene saponins obtained mainly from the plant ginseng. Several recent studies have reported that ginsenosides have a variety of pharmacological activities against several diseases including inflammation, cancer and cardiovascular diseases. This review focuses on describing the different pharmacological functions and underlying mechanisms of various active ginsenosides (Rb1,-Rd, -F, -Rg1, -Rg2, and -Rg3, and compound K) for atherosclerosis, which could provide useful insights for developing novel and effective anti-cardiovascular drugs.

• Biomolecules & Therapeutics
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• v.18 no.2
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• pp.135-144
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• 2010

The pro-oxidative and pro-inflammatory pathways in vascular endothelium have been implicated in the initiation and progression of atherosclerosis. In fact, inflammatory responses in vascular endothelium are primarily regulated through oxidative stress-mediated signaling pathways leading to overexpression of pro-inflammatory mediators. Enhanced expression of cytokines, chemokines and adhesion molecules in endothelial cells and their close interactions facilitate recruiting and adhering blood leukocytes to vessel wall, and subsequently stimulate transendothelial migration, which are thought to be critical early pathologic events in atherogenesis. Although interleukin-4 (IL-4) was traditionally considered as an anti-inflammatory cytokine, recent in vitro and in vivo studies have provided robust evidence that IL-4 exerts pro-inflammatory effects on vascular endothelium and may play a critical role in the development of atherosclerosis. The cellular and molecular mechanisms responsible for IL-4-induced atherosclerosis, however, remain largely unknown. The present review focuses on the distinct sources of IL-4-mediated reactive oxygen species (ROS) generation as well as the pivotal role of ROS in IL-4-induced vascular inflammation. These studies will provide novel insights into a clear delineation of the oxidative mechanisms of IL-4-mediated stimulation of vascular inflammation and subsequent development of atherosclerosis. It will also contribute to novel therapeutic approaches for atherosclerosis specifically targeted against pro-oxidative and pro-inflammatory pathways in vascular endothelium.