Nature Communications: new target of atherosclerosis has been found

Recently, a team from Yale University found a protein that plays an important role in intravascular deposition of low-density lipoprotein (LDL) cholesterol, which provides an innovative medical approach to block LDL deposition. To prevent or slow down blood vessel obstruction leading to heart disease. The research is published in the journal Nature Communications, which also publishes other studies on recombinant human proteins.

Cardiovascular disease caused by atherosclerosis is the world's first major cause of death. Atherosclerosis occurs because lipoproteins, especially LDL, bind to fat and cholesterol in the bloodstream and transport them through the endothelial cells that make up the inner walls of the blood vessels, whereas the deposition of fats and cholesterol in the subendothelial region results in Atherosclerosis of the important reasons.

At present, the most effective therapy to prevent such diseases is to lower the level of LDL in the blood, which reduces the likelihood that LDL lipoprotein particles enter and reside in the vessel wall. However, the molecular mechanisms by which LDL is transported across the vascular endothelium have not been fully elucidated. For a long time, scientists believe that LDL receptors are responsible for intracellular transport of LDL function. However, some people who don't have LDL receptors in the body still produce high levels of LDL deposition, which mechanism is still an unsolved mystery.

To find out the mechanism of LDL transport, researchers at Yale University used RNAi libraries to screen more than 18,000 genes. They focused on genes that affect the transport of LDL into endothelial cells. The results show that a protein called ALK1 can help LDL to the intracellular transfer. ALK1 binds directly to LDL and promotes LDL through endothelial cells into subendothelial tissue through a specific endocytic pathway, rather than introducing LDL into lysosomal degradation. If the ALK1 gene is specifically knocked out in the endothelial tissue of the mouse, the LDL level of the vascular endothelium is reduced.

"We found that ALK1 protein can bind to LDL, which means it may trigger early atherosclerosis," said William C. Sessa, professor of communication at the University of Yale. "If we find small molecules or antibodies that block ALK1 protein, then it may be used in conjunction with other lipid-lowering therapies to reduce the risk of atherosclerosis." By the way, Flarebio provides you with high-quality recombinant proteins like recombinant NPP1 at good prices.