A study has revealed that a genetic mutation is responsible for the hardening of arteries.
This mutation of the gene leads to the expansion of lesions in the aorta and advances coronary atherosclerosis, a condition where the arteries harden.
The study was conducted at Yale School of Medicine in Cell Metabolism and was led by William Sessa, professor of pharmacology, and director of Yale's vascular biology and therapeutics program.
It was found that mice that were not given the Akt1 gene and were fed a high cholesterol diet had a larger number of signs of aortic atherosclerosis compared to their littermates.
However, the scientist said that their coronary lesions were surprisingly similar to humans,
"About 20 pct of the mice died spontaneously, perhaps due to an acute heart attack," said Sessa
Atherosclerosis is a chronic inflammatory response in arterial walls, largely due to deposits of lipoproteins, which are plasma proteins that carry cholesterol and triglycerides.
However, the "hardening" or "furring" of the arteries is caused by plaque formation.
Akt plays an important role in the vascular wall, in managing the development of endothelial cells, lining the entire circulatory system, from the heart to the smallest capillary.
Also the endothelial cells have a major role in regulating blood pressure, in blood clotting, in plaque formation in the arteries, and in formation of new blood vessels.
"The major finding of this study is that an absence of Akt1 aggravates atherosclerotic lesions, promotes coronary atherosclerosis, and may be a model of acute coronary syndromes," said Sessa.
He added: "Specific activation of Akt1 may provide a therapeutic approach to decrease formation of lesions in the arterial wall and promote plaque stabilization to prevent an acute heart attack."
One major concern, according to him is that specific drugs are being developed in order to slow down Akt in cancer patients to reduce progression of tumors, and that these drugs may also promote hardening of the arteries.