A recent study by scientists at the Center for Research on Redox Processes in Biomedicine (Redoxoma) has shed light on why people with high blood sugar, often due to diabetes, are more likely to suffer from blood clots, a condition known as thrombosis.
These findings, published in the Journal of Thrombosis and Haemostasis, could help develop new ways to protect diabetics from heart attacks and strokes.
Thrombosis plays a major role in severe health issues like heart attacks and strokes, especially in places like Brazil and Latin America, where these conditions are leading causes of death. High blood sugar, or hyperglycemia, is a well-known risk factor for these cardiovascular diseases.
Renato Simões Gaspar, the study’s main author, pointed out that among various risk factors like high cholesterol and high blood pressure, hyperglycemia has a particularly strong link to heart problems.
This research, led by Dr. Francisco Laurindo from the University of São Paulo, looked specifically at how prolonged high blood sugar levels in diabetics lead to problems in blood vessel linings. Over time, high blood sugar damages the inner lining of blood vessels, called the endothelium.
This damage can trigger platelets—tiny blood cells responsible for clotting—to attach to the vessel walls, forming clots. These clots can block blood flow, causing heart attacks or strokes, which are extremely dangerous for those with diabetes.
A central finding of the study was how a specific protein, known as protein disulfide isomerase (PDI), is involved in this process. PDI normally exists within cells, where it helps proteins fold correctly.
However, it also exists outside the cell, known as peri/epicellular PDI (pecPDI), where it has other functions. The study showed that pecPDI helps regulate how platelets stick to the blood vessel walls in the presence of high blood sugar.
To better understand this, the researchers experimented with human cells exposed to different blood sugar levels. They used two groups of cells: one with normal glucose levels and another with high glucose levels.
When they introduced platelets from healthy individuals to these cells, they found that platelets attached to cells with high glucose levels three times more often than to cells with normal glucose levels.
However, when they used chemicals to block the activity of PDI, this effect was reversed, suggesting that pecPDI plays a significant role in platelet adhesion in high-sugar environments.
The study also revealed other changes in the cells exposed to high sugar levels.
The team noticed that cells in a high-glucose environment had a stiffer structure and produced more hydrogen peroxide, a reactive molecule that can alter cell behavior. These stiffer cells were more likely to attract platelets, increasing the risk of clots.
Using advanced imaging techniques, the researchers observed that cells in high-sugar environments formed small extensions that released tiny particles. These particles, known as extracellular vesicles, seemed to play a role in attracting platelets.
To understand this further, the team analyzed the proteins secreted by these cells and found nearly 1,000 different proteins in total. After focusing on those involved in cell adhesion, they identified two key proteins, SLC3A2 and LAMC1, which were linked to the increased platelet attachment.
The study’s findings underscore how prolonged high blood sugar can make blood vessels more likely to trap platelets, a process that pecPDI seems to regulate closely.
This knowledge is valuable because it could help scientists develop treatments to reduce clotting risks in people with diabetes, possibly by targeting PDI or the proteins it affects.
By understanding these mechanisms better, researchers hope to provide diabetics with more effective strategies to prevent blood clots, thereby reducing their risk of heart attacks and strokes. This research marks an important step in managing the health complications associated with diabetes.
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The research findings can be found in the Journal of Thrombosis and Haemostasis.
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