A new study from the University of Sydney’s Charles Perkins Centre has uncovered a biological clue that might explain why people with type 2 diabetes face a higher risk of dangerous blood clots.
The discovery could lead to future treatments that lower the risk of heart attacks and strokes in this growing population.
The research, published in the Journal of Clinical Investigation, was led by Associate Professor Freda Passam and Associate Professor Mark Larance. Their team focused on a protein called SEC61B, which they found to be significantly increased in the platelets of people with type 2 diabetes.
Platelets are tiny blood cells that help stop bleeding by forming clots, but in people with type 2 diabetes, they often become too active and form harmful clots inside blood vessels.
The study showed that SEC61B disrupts calcium levels within the platelets, making them more likely to clump together. This raises the risk of blood clots, which can lead to serious complications like heart attacks and strokes.
To test whether this protein could be targeted to reduce clotting, the researchers used an antibiotic called anisomycin. They found that blocking SEC61B with anisomycin reduced platelet clumping in both human samples and animal models.
“People living with type 2 diabetes are vulnerable to increased risk of blood clots,” said Associate Professor Passam. “These exciting findings identify a whole new way to reduce this risk and help prevent life-threatening complications like heart attack and stroke.”
According to statistics, nearly 1.2 million Australians were living with type 2 diabetes in 2021, with higher rates among Aboriginal and Torres Strait Islander communities and people in rural and regional areas.
Cardiovascular disease remains a leading cause of death for people with diabetes. Their heightened platelet activity makes standard blood-thinning treatments less effective, creating a need for better solutions.
Using advanced tools to study the proteins in platelets, the team discovered that SEC61B causes calcium to leak from storage areas inside the cells. This leakage increases platelet reactivity and the tendency to form clots.
Although treatments that target SEC61B are still in the early stages, the research team believes that testing in animals could start within a year or two. If successful, therapies for human patients could be available within the next decade.
This discovery opens up a promising new path for tackling cardiovascular risks in people with type 2 diabetes, offering hope for more targeted and effective treatments in the future.
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The study is published in the Journal of Clinical Investigation.
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