Endothelial dysfunction is driven by apo-b particle retention and oxidation, which further exacerbates these processes.

“so as the APO B particles get retained and oxidized and the immune cells namely macrophages um well monocytes that become macrophages undergo the phagocytosis of the oxidized LDL particles and become foam cells that creates sort of an inflammatory milieu in the sub endothelial space that increases more endothelial that you know sort of drives endothelial dysfunction and leads to a greater and greater Cascade of more apob particles being retained oxidized Etc”