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Lipoprotein-mediated cellular mechanisms for atherogenesis in hypertriglyceridemia
1Department of Medicine, Baylor College of Medicine, Houston, TX 77030.
Seminars in Thrombosis and Hemostasis
|April 1, 1988
Summary
Abnormal very-low-density lipoprotein (VLDL) in hypertriglyceridemia may cause atherosclerosis. These particles injure cells and form foam cells, potentially leading to arterial disease in vivo.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Lipid Metabolism
Background:
- Hypertriglyceridemia is associated with cardiovascular disease.
- Very-low-density lipoprotein (VLDL) metabolism is complex and not fully understood in disease states.
- Abnormal VLDL particles have been observed in hypertriglyceridemic individuals.
Purpose of the Study:
- To investigate the atherogenic potential of abnormal VLDL particles found in hypertriglyceridemia.
- To explore the interaction of abnormal VLDL with arterial cells and its in vitro effects.
- To hypothesize the in vivo mechanisms by which abnormal VLDL may contribute to atherosclerosis.
Main Methods:
- Characterization of VLDL structure and function in hypertriglyceridemic subjects.
- In vitro studies assessing VLDL interaction with endothelial cells and macrophages.
- Comparison of cholesterol content between VLDL and low-density lipoprotein (LDL) particles.
Main Results:
- Structurally and functionally abnormal VLDL particles are present in hypertriglyceridemia.
- These abnormal VLDL interact with cell surface receptors, unlike normal VLDL.
- In vitro, abnormal VLDL uptake damages endothelial cells and promotes foam cell formation in macrophages.
Conclusions:
- Abnormal VLDL particles are hypothesized to be atherogenic in vivo.
- Prolonged VLDL residence time and arterial cell interaction may promote endothelial injury.
- Initiation of foam cell formation by abnormal VLDL could contribute to atherosclerosis in hypertriglyceridemia.