The neat trick here is to restore
activity in dormant cells already in the heart.
It is presently no particular help for someone who has had a heart
attack, though that obviously could change as more work is done, but it is just
as obviously indicated for a patient that has suffered one heart attack.
Many of the patients suffering
from heart failure are in fact suffering from the damage inflicted by even
several attacks. If one can minimize the
effects of the first such attack, then been able to reverse the effects of late
attacks is a clear winner.
In the past month we have also
seen additional therapy for heart failure emerge from the labs. As stated this was considered
untreatable. We are now opening the
floodgates to major improvements on the outlook for heart failure. Millions presently are so diagnosed and
reversing this problem is a huge boon.
Drug makes hearts repair themselves
By James GallagherHealth reporter, BBC News
More people are surviving heart attacks, but that means more are living
with heart failure
The damage caused by a heart attack had previously been considered
permanent.
But a study in the
journal Nature showed the drug, thymosin beta 4, if used in advance
of a heart attack, was able to "prime" the heart for repair.
The British Heart Foundation described repair as the "holy grail
of heart research", but said any treatment in humans was years away.
Due to advances in health care the number of people dying from coronary
heart disease is falling.
But those living with heart failure are on the rise - more than 750,000
people have the condition in the UK
Wake up
The researchers at University College London
Deaths from coronary heart disease
1961 - 165,216
2001 - 117,743
2009 - 80,223
Estimated people living with heart failure
1961 - 100,000
1971 - 300,000
2010 - 750,000
Source: British Heart Foundation
In adults epicardium-derived progenitor cells line the heart, but
have become dormant.
Scientists used a chemical, thymosin beta 4, to "wake them
up".
Professor Paul Riley, from the University
College London
"We saw an improvement in the ejection fraction, in the ability of
the heart to pump out blood, of 25%."
As well as pumping more blood, the scar tissue was reduced and the
walls of the heart became thicker.
Peter Weissberg, medical director of the British Heart Foundation, said
he was "very excited" about the research but warned the scale of
improvement seen in animals was rarely seen in humans.
Epicardium derived progenitor cells (in red) lining the heart
However, he argued that even a small improvement would have a dramatic
impact on people's quality of life.
"A normal heart has lots of spare capacity. In patients with heart
failure it is working flat out just to sit down [and] it's like running a
marathon," he said.
"You could turn a patient from somebody who's gasping while
sitting in a chair to somebody who can sit comfortably in a chair."
Advance therapy
The mice needed to take the drug in advance of a heart attack in order
for it to be effective. As the researchers put it, "the priming effect is
key".
If a similar drug could be found to be effective in humans, then the
researchers believe it would need to be prescribed in a similar way to statins.
Professor Riley said "I could envisage a patient known to be at
risk of a heart attack - either because of family history or warning signs
spotted by their GP - taking an oral tablet, which would prime their heart so
that if they had a heart attack the damage could be repaired."
He said this could be available in 10 years.
The British Heart Foundation, which funded the study, said repairing a
damaged heart was the "holy grail" of heart research.
The results strengthened the evidence that drugs could be used to
prevent the onset of heart failure, it said.
De novo cardiomyocytes from within the activated adult heart after
injury
Nicola
Smart, Sveva
Bollini, Karina
N. Dubé, Joaquim
M. Vieira, Bin
Zhou, Sean
Davidson, Derek
Yellon, Johannes
Riegler, Anthony
N. Price, Mark
F. Lythgoe, William
T. Pu & Paul
R. Riley
Nature Received 16 March 2010, Accepted 13 May 2011, Published
online 08 June 2011
A significant bottleneck in cardiovascular regenerative medicine is the
identification of a viable source of stem/progenitor cells that could
contribute new muscle after ischaemic heart disease and acute myocardial
infarction1.
A therapeutic ideal—relative to cell transplantation—would be to stimulate a
resident source, thus avoiding the caveats of limited graft survival,
restricted homing to the site of injury and host immune rejection. Here we
demonstrate in mice that the adult heart contains a resident stem or progenitor
cell population, which has the potential to contribute bona fide terminally
differentiated cardiomyocytes after myocardial infarction. We reveal a novel
genetic label of the activated adult progenitors via re-expression of a key
embryonic epicardial gene, Wilm’s tumour 1 (Wt1), through priming by thymosin
β4, a peptide previously shown to restore vascular potential to adult epicardium-derived
progenitor cells2 with
injury. Cumulative evidence indicates an epicardial origin of the progenitor
population, and embryonic reprogramming results in the mobilization of this
population and concomitant differentiation to give rise to de novo cardiomyocytes.
Cell transplantation confirmed a progenitor source and chromosome painting of
labelled donor cells revealed transdifferentiation to a myocyte fate in the
absence of cell fusion. Derived cardiomyocytes are shown here to structurally
and functionally integrate with resident muscle; as such, stimulation of this
adult progenitor pool represents a significant step towards resident-cell-based
therapy in human ischaemic heart disease.
No comments:
Post a Comment