They have located the correct
tool and must now learn how to safely use it in every patient. The good news is that it is plausible that
folks with a damaged heart can look forward to outright internal restoration
sometime in the future and that basically provides hope for everyone dealing
with an impacted heart.
This means of course a decline in
the need for an outright heart transplant for a large number of patients.
It may also mean a recovery
protocol for congestive heart failure.
Even as our options for outright
replacement are seriously improving, it is good to see that a real healing
mechanism may get there sooner.
I presume this protocol can be
made to work elsewhere on less critical organs like scar damaged lungd.
Diseased Hearts to Heal Themselves in Future
ScienceDaily (Nov. 11, 2011) — Oncostatin M regulates the
reversion of heart muscle cells into precursor cells and is vitally important
for the self-healing powers of the heart.
Cellular reversion processes arise in diseases of the heart muscle, for
example myocardial infarction and cardiomyopathy, which limit the fatal
consequences for the organ. Scientists from the Max Planck Institute for Heart
and Lung Research in Bad Nauheim and the Schüchtermann Klinik in Bad
Rothenfelde have identified a protein which fulfils a central task in this
reversion process by stimulating the regression of individual heart muscle
cells into their precursor cells. They now plan to improve the
self-healing powers of the heart with the help of this protein.
In order to regenerate damaged heart muscle as caused by a heart
attack, for example, the damaged muscle cells must be replaced by new ones.
The number of cells to be replaced may be considerable, depending on the extent
of the damage caused. Simpler vertebrates like the salamander adopt a strategy
whereby surviving healthy heart muscle cells regress into an embryonic state.
This process, which is known as dedifferentiation, produces cells which contain
a series of stem cell markers and re-attain their cell division activity. Thus,
new cells are produced which convert, in turn, into heart muscle cells. The
cardiac function is then restored through the remodelling of the muscle tissue.
An optimised repair mechanism of this kind does not exist in humans.
Although heart stem cells were discovered some time ago, exactly how and to
what extent they play a role in cardiac repair is a matter of dispute. It has
only been known for a few years that processes comparable to those found in the
salamander even exist in mammals.
Thomas Braun's research group at the Max Planck Institute for Heart and
Lung Research in Bad Nauheim has now discovered the molecule responsible for
controlling this dedifferentiation of heart muscle cells in mammals. The
scientists initially noticed the high concentration of oncostatin M in tissue
samples from the hearts of patients suffering from myocardial infarction. It
was already known that this protein is responsible for the dedifferentiation of
different cell types, among other things. The researchers therefore treated
cultivated heart muscle cells with oncostatin M in the laboratory and were then
able to trace the regression of the cells live under the microscope:
"Based on certain changes in the cells, we were able to see that almost
all heart muscle cells had been dedifferentiated within six days of treatment
with oncostatin M," explains Braun. "We were also able to demonstrate
the presence of various stem cell markers in the cells. This should be understood
as an indicator that these cells had been switched to a repair mode."
Using a mouse infarct model, the Max Planck researchers succeeded in
demonstrating that oncostatin M actually does stimulate the repair of damaged
heart muscle tissue as presumed. One of the two test groups had been modified
genetically in advance to ensure that the oncostatin M could not have any
effect in these animals. "The difference between the two groups was
astonishing. Whereas in the group in which oncostatin M could take effect almost
all animals were still alive after four weeks, 40 percent of the genetically
modified mice had died from the effects of the infarction," says Braun.
The reason for this was that oncostatin M ensured clearly quantifiable better
cardiac function in the unmodified animals.
The scientists in Bad Nauheim would now like to find a way of using
oncostatin M in treatment. The aim is to strengthen the self-healing powers of
the damaged heart muscle and to enable the restoration of cardiac function for
the first time. The downside, however, is that oncostatin M was also observed
to be counterproductive and exacerbated the damage in an experiment on a
chronically diseased heart. "We believe that oncostatin M has considerable
potential for efficiently healing damaged heart muscle tissue. What we now need
is to be able to pinpoint the precise window of application to prevent any
possible negative effects," says Braun.
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Cellular regression in diseased heart tissue with the help of
oncostatin M: the image shows heart muscles under the fluorescence microscope.
The myofibrils are stained red, the cell nuclei blue.
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