Preventing a Broken Heart: Research aims to
reduce scarring from Heart Attacks
Newswise — A heart damaged by heart attack
is usually broken, at least partially, for
good. The injury causes excessive scar
tissue to form, and this plays a role in
permanently keeping heart muscle from
working at full capacity.
Now researchers have identified a key
molecule involved in controlling excessive
scar tissue formation in mice following a
heart attack. When they stopped the scarring
from occurring, the scientists found that
the animals’ heart function greatly improved
following the injury.
The study, by scientists at the University
of Wisconsin-Madison and Cornell University,
appears in Nature Cell Biology online Dec.
14, 2008.
The findings offer heartening news for the
millions who have heart attacks each year
and suffer from the resulting poor heart
function.
The study raises the hope that the outlook
for people with this major disability might
be markedly improved.
The scientists studied a protein, sFRP2,
which they unexpectedly found to be involved
in the formation of collagen, the main
component of scar tissue.
“With many injuries and diseases, large
amounts of collagen are formed and deposited
in tissues, leading to scarring and a
condition called fibrosis,” explains
co-author Daniel S. Greenspan, professor of
pathology and laboratory medicine at the UW
School of Medicine and Public Health.
“Fibrosis can seriously affect the
functioning of heart, lung, liver and other
tissues.”
Greenspan, an expert on collagen, joined
with Thomas Sato of Weill Cornell Medical
College to study mice that don’t produce
sFRP2 to understand how the protein works.
When the scientists restricted blood flow to
the animals’ hearts, mimicking a heart
attack, they found that scarring was
significantly reduced in these sFRP2-free
animals.
“Importantly, we found that when we reduced
the level of fibrosis, heart function
significantly improved in the mice,” says
Greenspan, also a professor of pharmacology
at UW-Madison.
Identifying agents that specifically target
sFRP2 and halt its activity will be a
promising approach to controlling heart
attack-induced scarring and impaired heart
function, says Greenspan, and his lab has
begun the search.
The UW scientists also hope to study how
sFRP2 and other proteins that enhance
collagen formation may interact.
The protein may also be important in
treating other diseases resulting in severe
fibrosis, adds Greenspan, including liver
cirrhosis and interstitial lung disease.
