Abnormal VLDL in hypertriglyceridemic patients interacts with cell surface receptors, causing endothelial injury and converting macrophages into foam cells in vitro, suggesting an atherogenic mechanism.
Abnormal VLDL in hypertriglyceridemia may promote atherogenesis through receptor-mediated endothelial injury and foam cell formation.
Structurally and functionally abnormal VLDL exist in hypertriglyceridemic humans. These large abnormal VLDL, in contrast to large normal VLDL, interact with cell surface receptors. One large VLDL particle carries far more total cholesterol than one LDL particle. Receptor-mediated uptake of abnormal VLDL is injurious to endothelial cells and converts macrophages into foam cells in vitro. These observations lead to the hypothesis that if similar phenomena occur in vivo, abnormal VLDL, which have prolonged residence times and increased opportunity to interact with arterial cells, are atherogenic by promoting endothelial injury and initiating foam cell formation. Since premature atherosclerosis is associated with some forms of hypertriglyceridemia and foam cells accumulate in certain hypertriglyceridemic subjects, similar events may indeed occur in vivo.
Gianturco et al. (Fri,) conducted a review in Hypertriglyceridemia. Abnormal VLDL vs. Normal VLDL was evaluated. Abnormal VLDL in hypertriglyceridemic patients interacts with cell surface receptors, causing endothelial injury and converting macrophages into foam cells in vitro, suggesting an atherogenic mechanism.