Progression and regression of human coronary atherosclerosis The role of lipoproteins, lipases and thyroid hormones in coronary lesion growth

Barth, Jacques D.; Jansen, Hans; Kromhout, Daan; Reiber, J. H. C.; Birkenhäger, J. C.; Arntzenius, A. C.

doi:10.1016/0021-9150(87)90093-1

Cited by 42 publications

(16 citation statements)

References 34 publications

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“…It has been reported that the extent of coronary atherosclerosis is inversely associated with hepatic lipase levels (37), and that atherosclerotic lesion progression is associated with lower hepatic lipase (38). In high-risk subjects with familial hypercholesterolemia, hepatic lipase was inversely associated with the amount of coronary calcification (39).…”

Section: Discussionmentioning

confidence: 99%

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

et al. 2002

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Type 1 diabetes is associated with coronary heart disease (CHD) and coronary artery calcification (CAC), a measure of subclinical CHD. The hepatic lipase gene promoter polymorphism (LIPC-480C>T) is a common variant affecting lipid metabolism. This study examined the relation between the LIPC-480C>T and CAC in type 1 diabetes. In the type 1 diabetic patients studied, 56% had CAC >0 Agatston units (AU). These subjects had a longer duration of diabetes (26.2 ؎ 1.3 vs. 17.8 ؎ 1.4 years; P < 0.001), lower HDL cholesterol levels (55.7 ؎ 2.4 vs. 61.0 ؎ 2.5 mg/dl; P ‫؍‬ 0.05), higher triglyceride levels (101 ؎ 17.3 vs. 66 ؎ 7.6 mg/dl; P < 0.05), and higher diastolic blood pressure (79.7 ؎ 1.0 vs. 76.0 ؎ 1.4 mmHg; P < 0.05). The LIPC-480 T allele was more common in subjects with CAC (frequency ‫؍‬ 0.31 ؎ 0.05 vs. 0.14 ؎ 0.04; P ‫؍‬ 0.006). The proportion with CAC was 44% in LIPC-480CC subjects, 71% in heterozygotes, and 83% in LIPC-480TT subjects (P < 0.01). LIPC-480 T allele frequency increased as the amount of CAC increased (P ‫؍‬ 0.007). LIPC-480 genotype was independently associated with the CAC (odds ratio ‫؍‬ 2.90, 95% CI 1.22-6.92, P < 0.05) after adjusting for duration of diabetes, age, sex, diastolic blood pressure, HDL cholesterol, and triglyceride levels. In conclusion, the LIPC-480C>T polymorphism was associated with subclinical CHD in type 1 diabetes. This genetic variant may identify subjects in which early intervention to prevent CHD may be appropriate.

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Section: Discussionmentioning

confidence: 99%

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

et al. 2002

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“…Hypothyroidism is known to be associated with accelerated atherosclerosis and coronary artery disease. 1,2 The Rotterdam study showed that subclinical hypothyroidism is a risk factor for atherosclerosis and myocardial infarction independently of total cholesterol level. 3 It was shown that more angiographic progression of coronary atherosclerosis was documented in patients with the lower serum thyroid hormone level after 2 years of observation.…”

mentioning

confidence: 99%

“…3 It was shown that more angiographic progression of coronary atherosclerosis was documented in patients with the lower serum thyroid hormone level after 2 years of observation. 2,4 These results suggest that thyroid hormone is protective against atherosclerosis; however, the molecular mechanism of antiatherosclerotic effects has remained to be elucidated.…”

mentioning

confidence: 99%

Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

Fukuyama

Ichiki

Imayama

et al. 2006

ATVB

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Objective-Although accumulating evidences suggest that impaired thyroid function is a risk for ischemic heart disease, the molecular mechanism of anti-atherosclerotic effects of thyroid hormone is poorly defined. We examined whether thyroid hormone affects signaling pathway of angiotensin II (Ang II), which is critically involved in a broad aspect of cardiovascular disease process. Methods and Results-3,3Ј,5-triiodo-L-thyronine (T3) did not show a significant effect on Ang II-induced activation of extracellular signal-regulated protein kinase or p38 mitogen-activated protein kinase in vascular smooth muscle cells (VSMCs), whereas T3 inhibited Ang II-induced activation of cAMP response element (CRE) binding protein (CREB), a nuclear transcription factor involved in the vascular remodeling process. Coimmunoprecipitaion assay revealed the protein-protein interaction between thyroid hormone receptor and CREB. T3 reduced an expression level of interleukin (IL)-6 mRNA, CRE-dependent promoter activity, and protein synthesis induced by Ang II. Administration of T3 (100 g/100 g for 14 days) to rats attenuated neointimal formation after balloon injury of carotid artery with reduced CREB activation and BrdU incorporation. Conclusion-These results suggested that T3 inhibits CREB/CRE signaling pathway and suppresses cytokine expression and VSMCs proliferation, which may account for, at least in part, an anti-atherosclerotic effect of thyroid hormone.

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“…Subjects with severe CAD were subjected to a strictly vegetarian diet for 2 years. HL activity determined at the end of the study period correlated positively with regression of coronary atherosclerotic lesion size ( r ϭ Ϫ 0.55) (14); it appeared to be the most important predictor of regression. However, during hypolipidemic treatment of hypertriglyceridemic CAD patients with a familial history of CAD who participated in the FATS study, Zambon and coworkers (19) found that a decrease in HL activity correlated with a decrease in coronary stenosis ( r ϭ 0.57).…”

Section: Human Studiesmentioning

confidence: 89%

“…Low HL activity has been reported in patients with clinically overt CAD (2,14,15). In a population of 200 men undergoing elective coronary angiography, the extent of CAD correlated inversely with HL activity ( r ϭ Ϫ 0.19, P Ͻ 0.001), indicating that approximately 4% of the variance in CAD could be explained by HL.…”

Section: Human Studiesmentioning

confidence: 93%

Hepatic lipase

Jansen

Verhoeven

Sijbrands

2002

Journal of Lipid Research

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119

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Hepatic lipase (HL) plays a role in the metabolism of pro-and anti-atherogenic lipoproteins affecting their plasma level and composition. However, there is controversy regarding whether HL accelerates or retards atherosclerosis. Its effects on different lipoprotein classes show that, potentially, HL may promote as well as decrease atherogenesis. Studies in animals with genetically modulated HL expression show that it depends on the model used whether HL acts pro-or anti-atherogenic. In humans, HL activity seems to correlate inversely with atherosclerosis in (familial) hypercholesterolemia, and positively in hypertriglyceridemia. In normolipidemia, HL activity is weakly associated with coronary artery disease (CAD). Genetically low or absent HL activity is usually associated with increased CAD risk, especially if plasma lipid transport is impaired due to other factors. Since HL promotes the uptake of lipoproteins and lipoprotein-associated lipids, HL may affect intracellular lipid content. We hypothesize that the prime role of HL is to maintain, in concert with other factors (e.g., lipoprotein receptors), intracellular lipid homeostasis. This, and the uncertainties about its impact on human atherosclerosis, makes it difficult to predict whether HL is a suitable target for intervention to lower CAD risk. First, the physiological meaning of changes in HL activity under different conditions should be clarified. -Jansen, H., A. J. M. Verhoeven, and E. J. G. Sijbrands. Many factors contribute to the development and progression of atherosclerosis. There are good reasons to believe that hepatic lipase (HL) is one of these factors. HL plays a role in the metabolism of several pro-and antiatherogenic lipoproteins. In humans, a change in HL activity is often associated with changes in the plasma level and composition of different lipoproteins, and with an increased or lowered risk of coronary artery disease (CAD). However, despite of extensive research during the last decade and the use of genetically modified animal models, the questions of whether HL is a pro-or anti-atherogenic enzyme, and whether we can or should modulate HL to decrease CAD risk, have not been unambiguously answered. In vitro and in vivo studies suggest the pro-as well as anti-atherogenic potential of HL ( Table 1 ). In recent studies, HL was identified as focal point in the development of CAD. However, the investigators came to opposite conclusions with regard to the influence of HL on atherogenesis. While Zambon and coworkers (1) concluded "regression of coronary atherosclerosis results from . . . a new pathway of HL-mediated (read decreased HL) improvement in LDL buoyancy," Dugi and coworkers (2) stated "Low hepatic lipase activity is a novel risk factor for coronary artery disease."In this review, we will summarize evidence that connects HL to CAD. We will discuss the potential impact of HL on CAD based on its proposed roles in (lipoprotein) metabolism. Finally, we will try to answer the question of whether or not modulation of HL expressi...

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Progression and regression of human coronary atherosclerosis The role of lipoproteins, lipases and thyroid hormones in coronary lesion growth

Cited by 42 publications

References 34 publications

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

Hepatic lipase

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Progression and regression of human coronary atherosclerosis The role of lipoproteins, lipases and thyroid hormones in coronary lesion growth

Cited by 42 publications

References 34 publications

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C&gt;T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C&gt;T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

Hepatic lipase

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A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes

A Common Promoter Polymorphism in the Hepatic Lipase Gene (LIPC-480C>T) Is Associated With an Increase in Coronary Calcification in Type 1 Diabetes