Treatment Speeds Recovery of Heart Muscle

Researchers have found that damage to heart tissue caused by oxygen deprivation during a heart attack may be reduced and repaired more quickly by treatment with the embryonic cardiac protein thymosin beta-4.

Investigators at the University of Texas Southwestern Medical Center (Dallas, USA) created a mouse model for heart attack by tying off the coronary arteries in a group of 58 experimental animals. Half of the group was then treated with injections of thymosin beta-4 while the rest of the mice received injections of saline solution.

Results published in the November 25, 2004, edition of Nature revealed that treatment with thymosin beta-4 reduced the number of muscle cells that died as a result of the "heart attack” and stimulated the recovery of muscle mass. The mode of action of thymosin beta-4 was shown to be through the formation of a functional complex with PINCH and integrin-linked kinase (ILK), resulting in activation of the survival kinase Akt (also known as protein kinase B). This activity at the molecular level resulted in increased rates of cardiomyocyte migration, survival, and repair.

"If the protein has a similar effect in humans as it does in mice, the impact by sheer volume is great--nearly 1 million people have heart attacks every year just in the United States,” said senior author Dr. Deepak Srivastava, professor of molecular biology and pediatrics at the University of Texas Southwestern Medical Center. "The delivery is very simple and avoids many of the problems of using stem cells.”



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University of Texas Southwestern Medical Center