in hardening of the arteries
A genetic mutation expands lesions in the aorta and promotes coronary atherosclerosis,
more commonly known as hardening of the arteries, according to a study by Yale School of Medicine researchers in Cell Metabolism.
The researchers found that mice engineered without the Akt1 gene and fed a
high cholesterol diet had many more signs of aortic atherosclerosis compared
to their littermates. And, surprisingly, their coronary lesions were similar
to humans, say the scientists.
“About 20% of the mice died spontaneously, perhaps due to an acute heart
attack,” says William Sessa, senior author of the study, professor of pharmacology,
and director of Yale’s vascular biology and therapeutics program.
Atherosclerosis is a chronic inflammatory response in arterial walls, in large
part due to deposits of lipoproteins — which are plasma proteins that
carry cholesterol and triglycerides. The “hardening” or “furring” of
the arteries is caused by plaque formation.
In the vascular wall, Akt1 plays an important role in regulating the development
of endothelial cells, which line the entire circulatory system, from the heart
to the smallest capillary. Endothelial cells play an important 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,” Sessa says. “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 concern, he notes, is that specific drugs are being developed to inhibit
Akt1 in cancer patients to reduce progression of tumors, and that these drugs
may also promote hardening of the arteries.
Co-authors include Carlos Fernandez-Hernando, Eric Ackah, Jun Yu, Yajaira Suarez,
Takahisa Murata, Yasuko Iwakiri, Jay Prendergast and Robert Miao, of Yale,
and Morris Birnbaum of the Howard Hughes Medical Institute and the University
of Pennsylvania School of Medicine.
— By Jacqueline Weaver
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