For example, cholesterol enters cells by receptor-mediated endocytosis. These LDLs bind to LDL receptors on cell membranes, initiating endocytosis. The LDL receptors are defective, so cholesterol cannot enter the cells by endocytosis and thus accumulates in the blood, contributing to the development of atherosclerosis. In a nongrowing cell, the amount of plasma membrane remains relatively constant. Vesicle fusion with the plasma membrane offsets membrane loss through endocytosis.
Vesicles provide a mechanism to rejuvenate or remodel the plasma membrane.