Researchers identify antioxidant mechanisms involved in protection against heart disease

Apr 30 2007

Zvonimir Katusic, M.D., Ph.D., and Mayo colleagues have identified antioxidant mechanisms essential for regenerative function of endothelial progenitor cells (EPCs).

“This work paves the way for successful harnessing of the therapeutic effect of EPCs in the prevention and treatment of cardiovascular diseases,” Dr. Katusic says. The study will be presented during the 2007 Experimental Biology meeting in Washington, D.C., on April 29.

EPCs move from the bone marrow into the bloodstream to repair the endothelium during a heart attack or stroke. The endothelium is a single layer of cells that line the inner surface of blood vessels. It protects tissues against the formation of blood clots in arteries and veins. If the endothelium is not working properly, patients are at risk for developing heart disease, stroke, peripheral vascular disease and venous thrombosis.

Normally, when EPCs move into the bloodstream, the body can restore cardiovascular functions that may have gone awry. EPCs are resistant to stress and are capable of repairing the endothelium even under conditions of extreme ischemia (inadequate supply of oxygen to an organ). But when EPCs are in insufficient supply, they are unable to protect the body from heart disease or stroke.

The antioxidant mechanism Dr. Katusic and colleagues identified includes enzymes that protect EPCs from oxidative stress in diseased arteries and veins. Oxidative stress is a consequence of the elevated
production of free radicals that are associated with the inability of the antioxidant system to prevent free radicals from imposing tissue damage.

These research findings will lead to improved understanding of the molecular design of EPCs, says Dr. Katusic, a specialist in cardiovascular pharmacology at Mayo Clinic's campus in Rochester, Minn.

The study was funded by the National Heart Lung and Blood Institute.