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Tsukuba, Japan - Atherosclerosis is the result of a buildup of lipids in the inner walls of blood vessels, and is a major cause of heart disease and stroke. In a new study, researchers from the University of Tsukuba discovered a novel role for cAMP responsive element-binding protein 3 like 3 (CREB3L3) in the development of atherosclerosis and identified a mechanism by which it exhibits protective effects against atherosclerosis.
Atherosclerosis is the detrimental result of long-time high blood lipid levels leading to a thickening of the inner walls of blood vessels through the formation of a so-called plaque. As a result, blood flow to the brain and heart may decrease over time, and once the plaque ruptures, platelets in the blood stream aggregate and clog the blood vessel as they try to repair the damage. While a number of proteins and mechanisms are known to play a part in the development of atherosclerosis, research is ongoing to fully understand this complex process. CREB3L3 is a transcription factor, which is a protein that binds to DNA and regulates gene expression in the liver and small intestine, and plays an important role in the hepatic triglyceride and glucose metabolism.