ROCHESTER, Minn. — Atherosclerosis is a disease in which arteries narrow due to plaques. That narrowing can lead to heart attacks and strokes — both of which are leading causes of death in the U.S. Now, in a paper published in Science, Mayo Clinic researchers and colleagues show that senescent cells drive plaque formation in animal models of atherosclerosis.
When stressed, healthy cells undergo senescence. In this process, cells are blocked from growing or dividing. The cells also release bioactive molecules called the senescence-associated secretory phenotype, or SASP. These molecules break down the normal tissue structure. They also attract immune cells that cause local inflammation.
Using three mouse models, the team, led by Mayo Clinic scientist Jan van Deursen, Ph.D., discovered that senescent cells have negative effects at all three stages of the disease process:
Based on their work, the authors conclude that senescent cells are key drivers of plaque formation and maturation.
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In addition to Dr. van Deursen and Childs, other authors are:
Funding for this research was provided by the Paul F. Glenn Foundation and the National Institutes of Health.
Drs. van Deursen and Campisi are scientific co-founders of Unity Biotechnology, a company developing senolytic medicines, including small molecules that selectively eliminate senescent cells.
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