2006
DOI: 10.1002/jcu.20233
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Role of hyperlipidemia in atherosclerotic plaque formation in the internal carotid artery

Abstract: Total serum cholesterol level seems to be an independent risk factor of atherosclerosis in the carotid artery.

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Cited by 25 publications
(15 citation statements)
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References 30 publications
(37 reference statements)
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“…Furthermore, the fact that triglyceride levels vary considerably within individuals makes it more difficult to evaluate them as a risk factor for atherosclerosis. Other studies have also demonstrated no significant association between triglycerides and carotid plaque after controlling for other lipid parameters and vascular risk factors [38,39]. …”
Section: Discussionmentioning
confidence: 96%
“…Furthermore, the fact that triglyceride levels vary considerably within individuals makes it more difficult to evaluate them as a risk factor for atherosclerosis. Other studies have also demonstrated no significant association between triglycerides and carotid plaque after controlling for other lipid parameters and vascular risk factors [38,39]. …”
Section: Discussionmentioning
confidence: 96%
“…Carotid artery lesion is a manifestation of atherosclerotic diseases and its coexistence with coronary artery disease (CAD) and peripheral artery disease is well known. Several factors have been associated with carotid atherosclerosis, including aging and male gender , hypertension hypercholesterolemia , diabetes mellitus , tobacco smoking , and chronic kidney disease .…”
Section: Introductionmentioning
confidence: 99%
“…Capitalizing on this new concept, we extend our mechanistic in vitro studies in vivo , and demonstrated herein that chronic injection of super-low dose LPS can sustain a “memory” low-grade pro-inflammatory state in liver tissues of high-fat diet fed ApoE −/− mice. We used the well-established steatosis-prone model of ApoE deficient mice, as previous studies suggest that hyperlipidemia is the critical “first hit” and an essential driver for the development of steatosis and atherosclerosis (34, 35), and that the low-grade circulatory inflammatory components are subsequent facilitators not capable of initiating the development of steatosis or atherosclerosis in the absence of hyperlipidemia. We employed the subclinical endotoxemia model with chronic injection of super-low dose endotoxin, compatible with circulating levels of endotoxemia reported in humans and experimental animals with chronic inflammatory diseases such as atherosclerosis and diabetes (36-39).…”
Section: Discussionmentioning
confidence: 99%