A recent study has suggested that it might be possible to
target other areas to lower cholesterol. Specifically, rather than aiming to
inhibit one of the key proteins once they are in the LDL receptors, the idea is
to address the transport mechanism that ensures that the protein reaches the
LDL receptors in the first place.
The study, which was published in
eLife, follows a string of previous
studies that have aimed to see what happens once the so-called SEC24A gene gets
de-activated in mice. The current study is particularly intriguing as it takes
the research one step further. Specifically, rather than just focusing on
deactivating the gene, the researchers also sought to block vesicles from
reaching LDL receptors. In order to do so, they isolated the so-called PCSK9
protein, which usually works by destroying the liver cells receptors of LDL
(low-density lipoprotein). The key findings indicated that the mice developed
normally, but that their plasma cholesterol levels had decreased by 45 per cent.
Based on this, the researchers urged that there be trials with humans to
establish whether a treatment can be made.
We can certainly understand why
the researchers would want this, as there are some patients who are resistant
to statins or cannot take them because of medical contraindications who would
benefit from an alternative treatment. Perhaps it could even be used as a
complement to optimise treatment for patients who are using statins.
Alternatively, it could develop into an alternative treatment that patients could
have as a result of informed choice.
Although
the findings sound promising, we would caution against any overly optimistic
conclusions at this stage. It is clear that extensive long-lasting studies with
humans need to be carried out. However, the progress from animal study to
clinical trial to market is time-consuming, expensive and not always fruitful.
Nevertheless, it is safe to say that the findings from this study can at the
very least prove fruitful to guide further theorising.