Studies have suggested that a form of so-called good cholesterol, or high-density lipoprotein, can become dysfunctional and instead of protecting against heart disease becomes a promoter of it, actively clogging up and hardening arteries.
Now, new research led by the Cleveland Clinic in the US has discovered the molecular process that makes "good" cholesterol start behaving badly. https://plus.google.com/b/117096478591416616884/117096478591416616884/posts
They found that Apolipoprotein A1 (apoA1), an important structural molecule that helps transfer cholesterol out of artery walls and send it to the liver for excretion, can become oxidized while in the artery wall. Once oxidized, it loses its protective properties and instead contributes to the development of coronary artery disease.
They describe their findings in a paper published online in Nature Medicine.
Senior author Stanley Hazen, section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart and Vascular Institute at the Cleveland Clinic, says:
"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."
Their findings help explain why, despite the fact extensive studies have reported how high-density lipoprotein (HDL) protects the heart, clinical trials of drugs to raise HDL levels have so far failed to show they significantly improve cardiovascular health.