28 January 2014

Bad good cholesterol

When "good" cholesterol becomes "bad"

Kirill Stasevich, Compulenta

Cholesterol floating in the blood is divided into "good" and "bad" – that is, the one that is part of high-density lipoproteins (HDL), and contained in low-density lipoproteins (LDL). Bad lipoproteins cause atherosclerotic deposits on the inner walls of blood vessels, so they say that it is necessary to increase the level of HDL in every possible way and reduce the level of LDL.

However, despite the fact that the benefits of high-density lipoproteins have been studied and confirmed by experiments in every possible way, all attempts to improve the condition of the heart and blood vessels with their help in clinical conditions have led to nothing. That is, the HDL level was increased, but there were no cardiovascular improvements. What is the matter here, the specialists of the Cleveland Hospital (USA) finally managed to find out.

One of the main proteins of high–density lipoproteins is apolipoprotein A1 (ApoA1). It collects cholesterol from the walls of the arteries and helps to pack it into a lipoprotein particle, which is then sent to the liver, one of the main centers of fat metabolism.

It would seem that it is to this protein that the vessels owe their health and the absence of atherosclerotic plaques. However, as Stanley Hazen and his colleagues have shown, with atherosclerosis, most of apolipoprotein A1 is oxidized by the enzyme myeloperoxidase, and, instead of maintaining vascular health, it begins to spoil them.

Oxidized ApoA1 provokes inflammation in the walls of blood vessels, and it just precedes the appearance of plaques clogging the lumen of the vessel.

It took researchers five years to develop a method that would allow tracking oxidized ApoA1; scientists describe how it oxidizes and how it spoils the walls of blood vessels in an article in Nature Medicine (Huang et al., An abundant dysfunctional apolipoprotein A1 in human atheroma). They confirmed their results with clinical data: among 627 cardiac patients, those who had a lot of spoiled HDL with oxidized ApoA1 felt the worst.

That is, if atherosclerosis has already begun, it is too late to increase the level of "good" lipoproteins: the disease will still turn them into "bad" ones. (Although we note that these lipoproteins are bad, as they say, in a different manner than low-density lipoproteins, which are bad in their original structure.)

This is not very good news for those suffering from atherosclerosis, but, on the other hand, these data give doctors another diagnostic marker by which to monitor the development of the disease, and another target on which to beat drugs.

Prepared based on Medical Xpress: Process that turns 'good cholesterol' bad discovered.

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