Receptor-mediated metabolism of lipoproteins, particularly involving macrophages and their receptors, is crucial in understanding atherosclerosis.

“when you have genetic polymorphisms like familial hypercholesterolemia which i believe is more than 2 000 different genetic polymorphisms that can result in elevated ldl there are many things going on in your ldl receptor metabolism at the level of the liver or also at the level of the endothelium or also at the level of the macrophages in the sub-intimal space within the arterial wall that could affect the way these cells take up and distribute ldl particles”

“I wondered how much immune cells rely on lipoproteins let me repeat that immune cells like macras which are nucleated uh cells so they also have a family of receptors including LDL receptors how much are they impacted by having these mutations like the this girl with homozygous FH because the reason for the higher LDL were these mutated LDL receptors that had poor binding cap capability they couldn't bind to LDL particles well if what I was telling you is true that cells are reliant on these lipoproteins and immune cells themselves can't connect to them does that impact their performance does that impact their capability to clear plaque things along those lines”

“there have been in vitro studies on macroasia cultured from lipo proteins oh did you find it you have this one in okay perfect yeah so these are these were cultured um macras from people at heterozygous FH and they found that indeed their uh receptor binding capability was altered and therefore they seem to almost have a compensatory up expression of other receptors because there are other redundancies there are other receptors that can handle um LDL particles uh that can handle modified LDL particles and so forth”