Some people smoke, eat unhealthily, shun exercise, yet manage to avoid the damaged arteries that are often the price of such a lifestyle. A built-in protective mechanism in the smooth muscle cells of the blood vessels discovered by University of Texas Health Science Center at Houston researchers may explain their good fortune.

A protein known to play a critical role in preventing cancer also is the driving force of a “growthostat” that limits the proliferation of vascular smooth muscle cells in a timely and surprising way, says Ken Fujise, M.D., associate professor of cardiology at UT Medical School and a researcher at the UT Institute of Molecular Medicine for the Prevention of Human Diseases (IMM).

“ Smooth muscle cells add integrity and strength to the blood vessel wall. In the human body, these cells also are quiescent, or asleep-- they do not grow,” Fujise explains. And for a very good reason: smooth muscle cell overgrowth would block the arteries.

A variety of stimuli can set these cells off on a dangerous growth spurt. Cholesterol and smoking will do it, as will diabetes, for example, Fujise says. When smooth vessel cells grow, they join with the fatty plaques caused by cholesterol to cause atherosclerosis, the hardening, thickening and stiffening of the blood vessel walls that can lead to heart attack or stroke. Cholesterol alone, Fujise notes, explains only about half of all atherosclerotic disease.

Protein p53:
The Plot Thickens

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