<unk>  particles are formed when triglycerides are removed from<unk>  by the lipoprotein lipase enzyme (LPL) and they become smaller and denser (i.e. fewer fat molecules with same protein transport shell), containing a higher proportion of cholesterol esters. Transport into the cell When a cell requires additional cholesterol (beyond its current internal HMGCoA production pathway), it synthesizes the necessary<unk>  receptors as well as PCSK9, a proprotein convertase that marks the<unk>  receptor for degradation.<unk>  receptors are inserted into the plasma membrane and diffuse freely until they associate with clathrin-coated pits. When<unk>  receptors bind<unk>  particles in the bloodstream, the clathrin-coated pits are endocytosed into the cell. Vesicles containing<unk>  receptors bound to<unk>  are delivered to the endosome. In the presence of<unk>  pH, such as that found in the endosome,<unk>  receptors undergo a conformation change, releasing<unk> .<unk>  is then shipped to the lysosome, where cholesterol esters in the<unk>  are hydrolysed.<unk>  receptors are typically returned to the plasma membrane, where they repeat this cycle. If<unk>  receptors bind to PCSK9, however, transport of<unk>  receptors is redirected to the lysosome, where they are degraded. Role in the innate immune system<unk>  interfere with the quorum sensing system that upregulates genes required for invasive Staphylococcus aureus infection. The mechanism of antagonism entails binding apolipoprotein B to a S. aureus autoinducer pheromone, preventing signaling through its receptor. Mice deficient in apolipoprotein B are more susceptible to invasive bacterial infection.<unk>  size patterns<unk>  can be grouped based on its size: large<unk>  density<unk>  particles are described as pattern A, and small high density<unk>  particles are pattern B. Pattern B has been associated by some with a higher risk for coronary heart disease. This is thought to be because the smaller particles are more easily able to penetrate the endothelium of arterial walls. Pattern I, for intermediate, indicates that most<unk>  particles are very close in size to the normal gaps in the endothelium (26 nm). According to one study, sizes 19.0–20.5 nm were designated as pattern B and<unk>  sizes 20.6–22 nm were designated as pattern A. Other studies have shown no such correlation at all. Some evidence suggests the correlation between Pattern B and coronary heart disease is stronger than the correspondence between the<unk>  number measured in the standard lipid profile test. Tests to measure these<unk>  subtype patterns have been more expensive and not widely available, so the common lipid profile test is used more often. There has also been noted a correspondence between higher triglyceride levels and higher levels of smaller, denser<unk>  particles and alternately<unk> er triglyceride levels and higher levels of the larger, less dense ("buoyant")<unk> . With continued research, decreasing cost, greater availability and wider acceptance of other lipoprotein subclass analysis assay methods, including NMR spectroscopy, research studies have continued to show a stronger correlation between human clinically obvious cardiovascular events and quantitatively measured particle concentrations. Oxidized<unk>  Oxidized<unk>  is a general term for<unk>  particles with oxidatively modified structural components. As a result from free radical attack, both lipid and protein parts of<unk>  can be oxidized in the vascular wall. Besides the oxidative reactions taking place in vascular wall, oxidized lipids in<unk>  can also be derived from oxidized dietary lipids. Oxidized<unk>  is known to associate with the development of atherosclerosis, and it is therefore widely studied as a potential risk factor of cardiovascular diseases. Atherogenicity of oxidized<unk>  has been explained by lack of recognition of oxidation-modified<unk>  structures by the<unk>  receptors, preventing the normal metabolism of<unk>  particles and leading eventually to development of atherosclerotic plaques. Of the lipid material contained in<unk> , various lipid oxidation products are known as the ultimate atherogenic species. Acting as a transporter of these injurious molecules is another mechanism by which<unk>  can increase the risk of atherosclerosis.
Low-density lipoprotein
High-density lipoprotein
Very low-density lipoprotein
Apolipoprotein
Intermediate-density lipoprotein
Lipoprotein
Cholesterol
Lipoprotein-X