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Researchers Discover Process That Turns 'Good’ Cholesterol Bad

Dysfunctional HDL promotes inflammation and coronary artery disease (January 26)

Cleveland Clinic researchers have discovered the process by which high-density lipoprotein (HDL) — the so-called “good” cholesterol — becomes dysfunctional, loses its cardioprotective properties, and instead promotes inflammation and atherosclerosis. Their research was published online in Nature Medicine.

The beneficial and cardioprotective properties of HDL have been studied and reported extensively, and yet all clinical trials of pharmaceuticals designed to raise HDL levels have failed to show that they significantly improve cardiovascular health.

This disconnect, as well as recent research showing that a protein abundant in HDL is present in an oxidized form in diseased artery walls, spurred the research team to study the process by which HDL becomes dysfunctional.

Apolipoprotein A1 (apoA1) is the primary protein present in HDL, providing the structure of the molecule that allows it to transfer cholesterol out of the artery wall and deliver it to the liver, from which cholesterol is excreted. The investigators discovered that in the artery wall during atherosclerosis, a large proportion of apoA1 becomes oxidized and no longer contributes to cardiovascular health, but rather, contributes to the development of coronary artery disease.

Over 5 years, the researchers developed a method for identifying dysfunctional apoA1/HDL and discovered the process by which it is oxidized and turned dysfunctional in the artery wall. They then tested the blood of 627 Cleveland Clinic cardiology patients for the dysfunctional HDL and found that higher levels raised the patients' risk for cardiovascular disease.

The research points toward new therapeutic targets for pharmaceuticals, such as those designed to prevent the formation of dysfunctional HDL and the development or progression of atherosclerosis, the authors say.

Source: EurekAlert; January 26, 2014.

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