The way in which high-density lipoprotein (HDL) – the so-called “good cholesterol” – becomes dysfunctional, it loses its protective properties cardiovascular, and instead promotes inflammation and atherosclerosis has been discovered by researchers at the Cleveland Clinic. The study results were published in the journal Nature Medicine .
process that converts the ‘good cholesterol’ Bad Identified
The beneficial properties and cardioprotective of HDL have been studied and widely reported, however, all clinical trials of pharmaceutical products to raise levels of HDL have so far not shown to significantly improve cardiovascular health. This disconnect, and recent research showing that an abundant protein in HDL is present in an oxidized form diseased artery walls, stimulated the research team – led by Stanley Hazen, MD, Ph.D., Vice President of Translational Research the Lerner Research Institute and section head of Preventive Cardiology and Rehabilitation at the heart and Vascular Institute Miller Family Cleveland Clinic – to study the process by which HDL becomes dysfunctional.
Apolipoprotein A1 (apoA1) is a major protein present in HDL, providing the structure of the molecule allows the arterial wall cholesterol is transferred and delivered to the liver, which is excreted cholesterol. ApoA1 is normally given HDL cardiovascular protective qualities, but Dr. Hazen and his colleagues have found that in the artery wall during atherosclerosis, a large proportion of apo A1 is oxidized and no longer contributes to cardiovascular health but rather, it contributes to the development of the disease of the coronary artery.
Over more than five years, Dr. Hazen and his colleagues developed a method to identify dysfunctional apo A1 / HDL and discovered the process by which it oxidizes and became dysfunctional in the wall of the artery. They then tested the blood of 627 patients of cardiology at the Cleveland Clinic for dysfunctional HDL and found that the highest levels increased a patient’s risk of cardiovascular disease.
“The identification of the structure of dysfunctional apoA1 and the process by which becomes instead of promoting disease prevention and disease-is the first step in creating new tests and treatments for cardiovascular disease,” said Dr. . Hazen. “Now we know what this dysfunctional protein seems, we are developing a clinical trial to measure its levels in the bloodstream, which will be a valuable tool both for assessing the risk of cardiovascular disease in patients and to guide the development of therapies for HDL to prevent disease. ”
The research also points to new therapeutic targets for pharmaceutical products such as those designed to prevent the formation of dysfunctional HDL and the development or progression of atherosclerosis.
This article was originally published on medindia.net
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