Researchers from the University of Texas Southwestern Medical Centre say that the formation of narrow blood vessels can lead to heart attack and strokes too. SR-B1 is a kind of protein which carries LDL particles over the endothelial cells which line the arteries. The study of how it carries the particles was published in the Nature journal.
In that study, it was also detected that a second protein known as dedicator of cytokinesis 4 or also called as DOCK4 are also associated with SR-B1 and also essential for the process. Dr. Philip Shaul, a senior author of the study said that the low-density lipoprotein which is commonly known as LDL cholesterol when enters into the artery wall leads to the growth of atherosclerosis or thickening of arteries. As a result of which, it turns into heart attacks and strokes. He also added that if treated in the future, to prevent the formation of these processes, it may help in reducing the occurrence of life-threatening state.
In the early stages of atherosclerosis what happens is that the LDL which enters in the artery wall attracts and is submerged by the vital immune system cells commonly known as macrophages which ingest or eats the LDL particles. These LDL laden macrophages become the foam cells which leads to swelling and the development of atherosclerotic plaques. These plaques narrow the arteries and become very unstable and the plaques which burst can trigger in the clotting of blood and can block the flow of blood towards the brain or heart. This can result in a stroke or heart attack.
In a recent study of mice with elevated cholesterol, the researchers said that the removal of SR-B1 from the cell resulted in the lessening of LDL entering the artery wall. This leads to the formation of lesser foam cells and smaller plaques. Dr. Shaul also mentioned that before working in this research the entry of LDL was unknown and thus the paper finding also solved the doubt of scientists LDL doesn’t enter through the damaged sites.
Scientists said that in their research they found out that atherosclerotic lesions are common due to the presence of more SR-B1 and DOCK4. To check if the same theory applies to human bodies the researchers viewed data on atherosclerotic and normal arteries from humans in three independent databases maintained by NIH. As a result, it was seen that SR-B1 and DOCK4 were huge in atherosclerotic arteries than normal ones.