Science News - October 22, 2011

mammalian heart can actually regenerate itself, the question becomes relatively easier,” Sadek says. “We can learn from the newborn heart.” He notes that his mouse research parallels the experience of doctors treating birth defects. Babies born with serious cardiac problems can recover completely if corrective surgery occurs shortly after birth. But if too many months pass before treatment, heart muscle is lost for good.

It’s not known why mammals would outgrow such a remarkable survival ability. (Some animals, including certain fish, enjoy a natural cardiovascular repair system for life.) Sadek speculates that during the course of evolution, before the human population lived long enough to grow old and have diseased arteries, a blow to the heart was usually fatal, so there wasn’t a need for a heart to heal. The challenge for scientists is to awaken a long-forgotten repair mechanism — whether by getting adult heart cells to return to their infancy or encouraging division and differentiation among a small population of existing heart stem cells.

at several points in life. “The difference between a newborn heart and an adult may focus on the ability of cells to divide, and not be related to their ability to create new DNA,” he says.

Epstein and others are trying to identify the genes and proteins necessary for a cell to take the additional step of cleaving itself in two once its DNA Clinical trials are already under way for drugs that inhibit Hdac enzymes, though investigating cancer treatment rather than heart disease. Animal studies have suggested that taking these drugs improves cardiac function after a heart attack or in the presence of high blood pressure — but the explanation for this benefit remains unclear.

Clinical trials are also in progress to
try to spur heart cell growth in people.
For the most part, researchers are test-
ing ways to give an ailing heart a dose of
a patient’s own bone marrow stem cells
with the hope that they will transform
into heart muscle, or revive cardiac
stem cells that might already lie inside.
The field got a kick start in 2001, when
Harvard. Using genes that give new
cells a telltale fluorescent glow, Lee’s
experiments suggest that after part of
the muscle dies, the heart makes a weak
attempt to mend. In mouse experiments
that mimic the damage of
a heart attack, more than

15 percent of the heart cells around the area of injury appear to be new, Lee and colleagues reported in 2007 in Nature Medicine. Later work supports that finding, he says.

“Our experiments sug-
gest that mammals like humans have
some repair capability,” he says. Recovery
happens, but “it is woefully inadequate.”
“It’s as if they try to re-enter the cell
cycle,” says Jonathan Epstein, scientific
director of the Penn Cardiovascular
Institute at the University of Pennsylva-
nia School of Medicine in Philadelphia.
“They make new DNA; they just don’t
divide.” It’s not uncommon for heart
cells to develop not just one but several
copies of their own genetic instruc-
tions, as if gearing up for the big event

“The totality of
evidence from
the clinical trials
is positive….
The heart is
pumping more
blood per beat.”

JOSHUA HARE

Divide and renew

Most scientists (though there are notable exceptions) have come to accept the idea that the heart contains stem cells, though there is no agreement on how plentiful or important they may be. (Estimates for the turnover of new heart muscle range from less than 1 percent per year to as much as 20 percent.)