Cardiac regeneration  pg. 4

A major obstacle is steering the cells to the desired location—the damaged heart tissue.

“In the clinical trials, in the best case scenario, no more than 3 percent to 4 percent of the cells reach the site,” says Hatzopoulos. “Most of them are lost in circulation.”

Confocal microscope image shows muscle cells developing within a cardiac infact, heart tissue that has died due to lack of oxygen.
Courtesy of Jan Kajstura, Ph.D., and Piero Anversa, M.D., Cardiovascular Research Institute, New York Medical College. Published in the Proceedings of the NationalAcademy of Sciences 102(24):8692-8697. Copyright 2005, National Academy of Sciences, U.S.A.
Hatzopoulos and colleagues have found that, after the ischemic event, there is an active interaction between bone marrow-derived cells and the vascular wall similar to the process seen when inflammatory cells migrate to a site of injury.

“During this process of ischemic injury, there is an upregulation of the inflammatory response,” he says. “Signals go out and mobilize a large number of cells from bone marrow—including monocytes, lymphocytes—but among them, there are cells that can participate more directly in tissue regeneration.”

The vascular wall also becomes active, or “sticky,” and captures these cells.

“The problem is that this upregulation of the ‘sticky’ vascular wall is a transient event—it happens within the first couple of days after injury and dies off,” Hatzopoulos continues.

It’s impractical to inject the cells that early “because they will be coming into a very hostile environment, so their survival is going to be very limited.” But if they’re injected a week later or a month later, “this area is not going to capture cells.”

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