English

Atherosclerosis affects millions of individuals each year, particularly those with insulin resistance and diabetes. It results from the accumulation of lipids and cholesterol in arterial vessels that lead to the formation of obstructive deposits. These deposits, known as plaques, limit the vital flow of oxygenated blood to organs and tissues. 

The damage resulting from atherosclerosis depends on the location of these deposits. 

• If they limit the blood flow to the heart, they may cause chest pain, and heart attacks. 
• If they limit blood flow to the brain, they may lead to stroke. 
• The plaques can cause an array of conditions, such as kidney disease, erectile dysfunction and even numbness in the limbs. 

Atherosclerosis is traditionally treated by reducing the amount of LDL or ‘bad cholesterol’ in the bloodstream. However, recent research has shown that other forms of cholesterol, such as remnant cholesterol, can also lead to Atherosclerosis.

So, a team of scientists from Canada and Cuba have joined forces in a historical collaboration to offer a novel approach. 

Rather than targeting just LDL cholesterol, the team aims to block all cholesterol from binding to specific sticky regions in the blood vessels known as glycosaminoglycans or GAGs. GAGs are sugar side chains in the artery walls that act as sticky regions for cholesterol particles. There is currently no class of drugs that prevents cholesterol from attaching to GAGs on the blood vessels.

However, pioneering scientists at the Centre for Molecular Immunology (CIM) in Cuba have developed an antibody known as chP3R99, which binds to the sugar side chains, effectively preventing cholesterol particles from forming plaques on the blood vessels. This mechanism is of great relevance to people with insulin resistance and diabetes, because the risk of cardiovascular disease is increased, partly due to a greater abundance of GAGs on the arterial wall.  

The treatment has shown promising results in preclinical models of atherosclerosis. 

What sets apart the drug developed at the CIM from other compounds is that while other treatments are usually only prescribed once risk is very high or plaque development can be seen clinically (late stages), the chP3R99 antibody has the potential to be effective across many stages of atherosclerosis development.

Moreover,  the antibody has a dual mechanism: not only does it bind to the GAGs sugar chains, but it does so in a vaccine-like fashion; once injected, it produces a cascade of secondary antibodies, which continue to exert the protective action against the accumulation of cholesterol.

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These scientists are confident that the treatment will soon prove to be effective against human arterial tissue.  

The collaborating teams hope to 

• corroborate their findings with in vivo and clinical studies,
• map in detail the mechanism of binding of the novel antibody to GAGs, specifically under conditions of insulin resistance, and 
• confirm that the antibody inhibits both remnant and LDL cholesterol in humans.  

If this is confirmed, the drug will undergo phase 1 clinical trial, offering new hope of long-time protection for millions of individuals with cardiovascular disease. 

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