A clearly promising drug regimen
although I cannot help but think that we are adjusting a secondary while not
clearly able to determine a real cause and affect protocol. In the meantime I suspect most heart patients
will support this new medicine.
It does solve the problem of
increasing the so called good cholesterol.
That alone may have an excellent effect of the likely prognosis. Yet the fact is that we do not know the causative
pathways and it could be a false lead.
We shall see as it tracks into
human testing.
New Therapy Shows Promise for Treating Cardiovascular Disease
ScienceDaily (Oct. 28, 2011) — A new therapy being studied in
non-human primates by researchers at Wake Forest Baptist Medical Center and
colleagues is demonstrating promise as a potential tool for combating
cardiovascular disease by increasing good cholesterol and lowering
triglycerides in the blood.
Supported by the National Institutes of Health and the Canadian
Institutes of Health Research, the preclinical findings appear in this week's
issue of the journal Nature.
"The study was conducted because there is a very strong inverse
correlation between the amount of HDL (good cholesterol) and heart
disease," said co-principal investigator Ryan Temel, Ph.D., an assistant
professor of pathology and lipid sciences at Wake Forest
Baptist. "The higher your level of HDL, the lower your risk of developing
cardiovascular disease. Currently, however, there are few therapies that
significantly raise HDL."
While there are several effective therapies available on the market for
lowering LDL, or bad cholesterol, modern medicine has yet to find a good way to
raise HDL, Temel said. "Even if you take a statin or some other therapy to
lower your LDL, the risk of having coronary heart disease is still around 50
percent. There's clearly a lot of room left for improvement."
Temel and colleagues from NYU Langone Medical Center and Regulus
Therapeutics Inc., a biopharmaceutical company, are studying a new drug that
targets microRNA-33 (miR-33). MiR-33 is a small RNA molecule that reduces HDL
and increases triglyceride production. In previous studies in mice, the drug
has been effective in promoting atherosclerotic plaque regression and
increasing HDL.
For the current study, researchers tested the drug, anti-miR-33, in
non-human primates and found that it increased HDL cholesterol and lowered
triglycerides. Non-human primates were selected this time because rodents only
express one form of miR-33 -- miR-33a -- while humans and non-human primates
have two types of miR-33 -- miR-33a and miR-33b.
In the study, use of the drug resulted in a maximum HDL cholesterol
increase of 50 percent after eight weeks that was sustained throughout the
remainder of the 12-week study. Anti-miR-33a/b treatment in the non-human
primate model also increased the expression of miR-33 target genes involved in
fatty acid breakdown resulting in suppressed triglyceride levels, a finding not
previously observed in mice. The decrease in triglycerides was apparent after
four weeks and reached a maximum reduction of 50 percent.
This pre-clinical study was the first to demonstrate that inhibiting
miR-33a/b has a significant and sustained effect on both circulating HDL and
plasma triglyceride levels, Temel said.
These findings indicate that miR-33a and miR-33b are key regulators of
cholesterol and fatty acid metabolism, Temel added, and that an anti-miR-33
approach could directly impact atherosclerosis, as well as address important
cardiovascular risk factors such low HDL and high triglycerides.
The researchers will next evaluate whether the drug has the ability to
stimulate cholesterol movement out of the arteries, where it has accumulated
and formed atherosclerotic lesions.
"Coronary artery disease is the number one killer of people in the
United States ,"
Temel said. "It's a very big problem. The ideal therapy would not only
reduce cholesterol accumulation in the arteries by lowering bad cholesterol but
also increase the removal of existing cholesterol in the arteries by elevating
good cholesterol. The combination of a statin and anti-miR-33 could potentially
be this therapy. While there is still a lot of work that needs to be done with
this drug before it can ever be used in humans, anti-miR-33 is showing strong
potential as a new therapy for reducing coronary heart disease risk."
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