An Akt against heart disease

As blood courses through the 100,000 miles of vessels in an adult’s circulatory system, cholesterol, fats and other debris can coat the walls of arteries, forming the dangerous, rupture-prone plaques of atherosclerosis. Scientists believe that atherosclerosis begins after damage to the endothelium, the innermost layer of cells that lines artery walls, but they are still learning about the genes that prevent—or promote—its progression.

In the December issue of Cell Metabolism, a team led by William C. Sessa, Ph.D., professor of pharmacology and director of the medical school’s program in Vascular Biology and Therapeutics, describes a key gene in the development of coronary atherosclerosis.

In mice prone to atherosclerosis, the loss of the gene Akt1 decreased endothelial production of the gas nitric oxide, leaving the endothelium even more susceptible to damage and the formation of fatty plaques. Mice lacking Akt1 also had more plaques in the aorta and coronary arteries, making them a valuable new model to understand acute coronary syndromes, such as unstable angina and heart attacks, in humans.