The discovery of a new biological pathway may explain why people with type 2 diabetes are twice as prone to dangerous blood clots—putting them at risk of heart attack and stroke.
This is the conclusion of researchers from the University of Sydney, who say their findings may pave the way for new treatments that reduce this danger.
“People with type 2 diabetes have a higher risk of heart attacks and strokes. Part of the reason for this is that their platelets are hyper-reactive,” paper author and hematologist professor Freda Passam told Newsweek.
Platelets are small cell fragments found in our blood that form clots to help stop bleeding. The high levels of blood sugar seen in diabetes, however, cause biochemical changes that make them “stickier”, Passam explained, so they can clot when not needed to.
The hematologist continued: “Drugs like aspirin prevent platelets from clotting, but are three times less effective in people with type 2 diabetes. Understanding why platelets are more active in diabetes opens the door to develop drugs that target this newly discovered pathway.”
In their study, the team found that the levels of a protein called “SEC61B” is significantly increased in the platelets—the tiny blood cells that help form clots—of people with type 2 diabetes.
The protein appears to disrupt calcium balance inside platelets, making them more likely to clump together and form clots, the researchers explained.
The researchers found that blocking SEC61B activity with an antibiotic called anisomycin reduced platelet clumping in both human samples and animal models.
Around 1 in 10 Americans (more than 38 million people) live with diabetes, of which 90–95 percent have type 2, which occurs when insulin doesn’t work properly or there’s not enough of it.
While type 2 diabetes typically develops in people aged 45 and over, children, teens and young adults are increasingly developing the condition as well.
“People living with type 2 diabetes are vulnerable to increased risk of blood clots,” Passam said in a statement. “These exciting findings identify a whole new way to reduce this risk and help prevent life-threatening complications like heart attack and stroke.”
In their study, the team analyzed both human and mouse platelets, discovering that SEC61B contributes to calcium leakage from the platelets’ stores, making the cell fragments more reactive.
The Australia-based researchers noted that the condition is “more prevalent in Aboriginal and Torres Strait Islander peoples and in rural and regional communities.”
“Cardiovascular disease is a leading cause of death in this group, partly due to the heightened activity of platelets—the tiny blood cells that help form clots,” they explained.
“This heightened platelet sensitivity to clotting also makes traditional anti-coagulant treatments less effective in people with type 2 diabetes, limiting the options to reduce the risk of cardiovascular disease.”
Treatments targeting SEC61B are still in early stages. However, the researchers believe pre-clinical trials in animals could begin within 1–2 years, with potential therapies for patients likely to be available in the next decade.
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Reference
Kong, Y. X., Rehan, R., Moreno, C. L., Madsen, S., Zhang, Y., Zhao, H., Qi, M., Houlahan, C., Cartland, S. P., Robertshaw, D., Trang, V., Ong, F. J. L., Liu, M., Cheng, E., Alwis, I., Dupuy, A., Cielesh, M., Cooke, K. C., Potter, M., Stӧckli, J., Morahan, G., Kalev-Zylinska, M., Rondina, M. T., Schulman, S., Yang, J., Neely, G. G., Schoenwaelder, S., Jackson, S., James, D., Kavurma, M. M., Hocking, S., Twigg, S. M., Weaver, J., Larance, M., & Passam, F. H. (2025). SEC61B regulates calcium flux and platelet hyperreactivity in diabetes. Journal of Clinical Investigation. https://doi.org/10.1172/JCI184597
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