By Medical Discovery News
Nov. 26, 2011
The vast majority of human cells regenerate: skin, stomach lining, red blood cells, bone cells, liver cells and the list goes on. But certain cells either do not regenerate at all, or take years to do so. Among these cells is a heart muscle cell called cardiomyocyte.
Starting at birth, these cells regenerate at just one percent a year, and by the time of death only half of the original heart muscle cells are replaced. That’s why damage from a heart attack is considered permanent. Within minutes, depending on where the blockage occurred, cardiomyocytes are either damaged or dead from a lack of oxygen-rich blood. The heart begins to produce replacement cells, but not fast enough. So, instead of new muscle cells, scar tissue forms, compromising the heart’s ability to pump blood. The amount of lost pumping ability depends on the size and location of the scar.
Scientists have spent years looking for a way to stop, slow or heal this damage, and they’re making headway. Researchers at the University of Texas Southwestern Medical Center in Dallas are focused on a small protein called Thymosin beta-4, or TB4. When the heart develops inside a human embryo, TB4 is made. This protein encourages the growth of cardiomyocytes, and stimulates the growth of blood vessels. Could this protein be used somehow to heal a damaged heart? Research with mice show this may be a promising new therapy.
Scientists have known the outer layer of the heart holds heart progenitor stem cells from which new cardiac cells are produced. They’re called epicardium-derived progenitor cells or EDPCs . These cells are usually dormant, but the UT researchers found when they injected the mice with TB4 it gave EDPCs a jump start. Within 24 hours, TB4 not only began to reduce the number of cardiomyocytes killed during a heart attack, but it also stimulated dormant progenitor cells to regenerate those that did die, reducing scar formation.
Over the long term, the mice also showed new blood vessel formation in the heart, bypassing blocked vessels. The hope is TB4 will prove to be just as effective in larger mammals and eventually, humans. Ideally, high risk patients would be treated prior to developing a heart attack as a preventative to prime the heart for repair, and possibly to treat the heart after an attack as well.
TB4 is already in clinical trials, and studies are also in progress to find molecules with the same but even more potent and specific effects. The goal among researchers is to provide TB4 or a drug with similar effects to the public in 10 years. In America alone, one million people suffer heart attacks every year and that number is only expected to grow.
Pamela K. Bond 