A team of researchers has discovered a process by which high-density lipoprotein (HDL) - known as 'good cholesterol' - becomes dysfunctional, loses its cardio-protective properties, and instead turns to 'bad cholesterol', thus promoting inflammation and atherosclerosis, or the clogging and hardening of the arteries.
Stanley Hazen, M.D., Ph.D., Vice Chair of Translational Research for the Lerner Research Institute and section head of Preventive Cardiology and Rehabilitation in the Miller Family Heart and Vascular Institute at Cleveland Clinic studied 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.
It's apoA1 that normally gives HDL its cardio-protective qualities, but Hazen and his colleagues 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 the course of more than five 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.
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They then tested the blood of 627 Cleveland Clinic cardiology patients for the dysfunctional HDL and found that higher levels raised the patient's risk for cardiovascular disease.
"Identifying the structure of dysfunctional apoA1 and the process by which it becomes disease-promoting instead of disease-preventing is the first step in creating new tests and treatments for cardiovascular disease," said Dr. Hazen.
The study was published in the journal Nature Medicine.
