Want good cholesterol? Then this latest study may just tell you how you attain it--and how you lose it, as well. Scientists have discovered the process by which high-density lipoprotein (HDL), so-called "good cholesterol," becomes dysfunctional and eventually promotes the clogging and hardening of arteries.
HDL has both beneficial and cardio-protective properties. Yet while researchers have attempted to create pharmaceuticals to raise HDL levels in the past, they have so far failed to significantly help improve cardiovascular health. Intrigued by this apparent anomaly, the researchers in this latest study decided to investigate a bit further to see how HDL becomes dysfunctional and might actually hurt your health.
Apolipoprotein A1 (apoA1) is the primary protein present in HDL. It provides the structure of the molecule that allows it to transfer cholesterol out of the artery wall and deliver it to the liver. There, cholesterol is excreted. In this latest study, though, researchers found that in the artery wall during atherosclerosis, a large proportion of apoA1 becomes oxidized and no longer contributes to cardiovascular health. Instead, it contributes to the development of coronary artery disease.
So how exactly does this happen? Over five years, the researchers developed a way for identifying dysfunctional apoA1/HDL and discovered the process by which it's oxidized and becomes dysfunctional.
"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 Stanley Hazen, one of the researchers, in a news release. "Now that we know what this dysfunctional protein looks like, we are developing a clinical test to measure its levels in the bloodstream, which will be a valuable tool for both assessing cardiovascular disease risk in patients and for guiding development of HDL-targeted therapies to prevent disease."
The findings reveal potential new therapeutic targets for pharmaceuticals. This could potentially help increase good levels of HDL and prevent the formation of dysfunctional HDL in the future.
The findings are published in the journal Nature Medicine.
