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Anti-inflammatory drug reduces vessel disease in diabetes

Professor Karlheinz PeterScientists have discovered a novel drug target to help stop some of the most common and deadly complications of diabetes, including heart attack and stroke.

The most common complications of diabetes stem from the damage that high blood sugar (hyperglycaemia) does to the body’s blood vessels.

Elevated blood sugar can damage the inner wall of blood vessels, setting off a domino effect of chronic inflammation, oxidative stress and then atherosclerosis — the build-up of plaques on the artery walls, which can restrict blood flow to the heart or rupture to form deadly blood clots.

People living with diabetes have up to a four-fold increased risk of heart attack than those without diabetes, because of this increased prevalence of atherosclerosis.

Now for the first time, a team of scientists from Baker Heart and Diabetes Institute’s Oxidative Stress lab have shown that by targeting chronic inflammation with a specific ‘small molecule inhibitor’ diabetes-associated vessel disease can be stopped in its tracks.

The preclinical research, recently , shows this targeted anti-inflammatory therapy can almost halve the signs of vessel disease.

Led by , Head of the Baker Institute’s Oxidative Stress laboratory, the testing in animal models showed diabetes increased atherosclerotic plaques four-fold, but these were reduced by about 40 per cent with drug treatment.

Results showed the drug reduced the development of harmful plaques, promoted plaque stability (leaving them less likely to rupture and cause a blood clot) and improved the overall function of blood vessels.

Professor de Haan said her evidence showed the drug could significantly slow the progression of vessel disease, preventing heart attack and stroke.

“It would allow clinicians to intervene as soon as they see early signs of diabetic vessel disease, such as build-up of plaque in the arteries of the lower limbs or even chest pain or angina, where there’s already a narrowing of vessels. They could then use the drug to stop the atherosclerotic plaques from growing bigger, or even prevent them from deadly rupture.”

/Baker Institute Public Release. View in full .