Researchers in Sydney have made a groundbreaking discovery, identifying a protein that explains why people with type 2 diabetes have a much higher risk of dangerous blood clots. This finding could lead to new therapies to prevent heart attacks and strokes, offering hope to millions worldwide. The study, led by Professor Freda Passam, pinpoints a new target for medications that could be more effective than current options like aspirin.
Why Blood Clots are a Major Risk in Diabetes
People with type 2 diabetes are about twice as likely to have a life-threatening heart attack or stroke compared to those without the condition. This increased risk is largely due to changes in their blood platelets, the tiny cell fragments responsible for clotting.
In a person with diabetes, high blood sugar levels alter the chemistry of platelets, making them overly “sticky.” This causes them to clump together inside arteries when they are not supposed to, forming blockages that can be deadly.
This is a critical problem because common blood-thinning drugs are not as effective in these patients. Professor Freda Passam, a leading hematologist, highlighted that aspirin is three times less effective for individuals with type 2 diabetes, leaving them vulnerable even while on treatment.
The Newly Discovered Protein, SEC61B
The research team identified a specific protein, SEC61B, that is present in much higher levels in the platelets of people with type 2 diabetes. This protein disrupts the delicate calcium balance within the platelets.
Since calcium is a key signal for activating platelets, this imbalance essentially puts them on constant high alert. The result is platelets that are far more prone to clumping and forming dangerous clots.
- Higher Levels: SEC61B is found in significantly higher amounts in diabetic platelets.
- Calcium Imbalance: It interferes with calcium regulation, a crucial part of clot formation.
- “High Alert” State: This keeps the platelets hyperactive and ready to form clots.
Crucially, the scientists found that they could reduce this hyperactivity. By using an antibiotic called anisomycin to block SEC61B, they successfully lowered platelet activity in both human blood samples and mouse models. This demonstrates that the pathway can be targeted with medication.
How This Discovery Changes the Game
For years, doctors have relied on standard anti-clotting medications like aspirin to manage cardiovascular risk. However, their reduced effectiveness in diabetic patients has been a major clinical challenge. These drugs often fail to fully control the heightened platelet activity seen in type 2 diabetes.
This discovery of SEC61B opens up a completely new avenue for treatment. Instead of trying to make existing drugs work harder, scientists can now develop therapies that target the root cause of the problem in these patients. It is like fixing a faulty switch rather than just trying to dim a light that is stuck on.
What This Means for Future Treatments
While this breakthrough is exciting, a therapy based on targeting SEC61B is not yet available. The researchers estimate that pre-clinical trials in animals could begin within the next one to two years. If those are successful, it could still be a decade before a treatment is ready for patients.
Medical research is a slow and careful process focused on ensuring safety and effectiveness. However, this finding provides a clear and promising direction. For the millions of people living with type 2 diabetes, it represents a significant step toward better prevention of its most serious complications.
| Statistic | The Impact on Type 2 Diabetes Patients |
|---|---|
| Cardiovascular Risk | Twice as likely to suffer a heart attack or stroke. |
| Aspirin Effectiveness | Three times less effective at preventing clots. |
| Prevalence in the US | 1 in 10 Americans has diabetes, with 90-95% being type 2. |
The urgency for new treatments is clear. This research could eventually reshape how doctors manage one of the deadliest risks associated with diabetes.
