Heart attacks and strokes are among the leading causes of death worldwide. In most cases, these serious medical emergencies happen when blood vessels become narrowed or blocked, preventing oxygen-rich blood from reaching vital organs such as the heart or brain.
The underlying problem often begins many years earlier with a condition called atherosclerosis. This disease develops slowly as fatty substances, including cholesterol, build up inside artery walls.
Over time, these deposits form plaques that can narrow blood vessels and reduce blood flow. If a plaque suddenly ruptures, a blood clot can form and completely block the artery, leading to a heart attack or stroke.
Scientists have known for many years that cholesterol is not the only factor involved in atherosclerosis. The immune system also plays a major role.
Researchers at Ludwig Maximilian University of Munich (LMU) have now uncovered new details about how certain immune cells influence the growth and stability of these dangerous plaques. Their findings may eventually lead to new treatments that lower the risk of cardiovascular disease.
The study focused on macrophages, a type of immune cell often described as the body’s cleanup crew. Macrophages normally help remove germs, dead cells, and unwanted material from tissues. In atherosclerosis, however, they become deeply involved in plaque formation.
As cholesterol accumulates inside artery walls, macrophages move into the area and begin swallowing the fat. Over time, these cells become overloaded with cholesterol and eventually die. The remains of dead cells and stored fats contribute to the growth of plaques.
Researchers have long studied these fat-filled macrophages, but the LMU team discovered that another group of macrophages may be equally important. These are macrophages that do not contain large amounts of fat.
Using advanced four-dimensional imaging techniques in mice, the researchers observed how different macrophage populations behave inside plaques. They found that lipid-free macrophages perform two very different functions.
On one hand, these cells help protect blood vessels. They remove cellular debris, including DNA released from dead cells. This cleanup process helps prevent the formation of cholesterol crystals. Cholesterol crystals are particularly dangerous because they can make plaques more unstable and increase the risk of blood clots.
On the other hand, the same macrophages can also damage the endothelium, the thin layer of cells that lines the inside of blood vessels. The endothelium plays a critical role in maintaining healthy blood flow and protecting artery walls.
This discovery highlights the complicated nature of inflammation in atherosclerosis. Inflammation is often viewed as harmful, but the study shows that some inflammatory processes may also help limit plaque growth and remove dangerous debris.
At the center of this balancing act is a tiny molecule known as miR-147. This molecule belongs to a group of molecules called microRNAs, which help control how genes function inside cells. Although microRNAs are extremely small, they can have powerful effects on biological processes.
The researchers found that miR-147 is produced mainly by lipid-free macrophages. It appears to help these cells perform their cleanup duties while reducing their harmful effects on blood vessels.
When the scientists removed miR-147, the results were dramatic. Plaques became larger, cholesterol crystals increased, and more DNA debris accumulated inside the arteries. These changes are all associated with a higher risk of cardiovascular complications.
Further investigation revealed that miR-147 works by suppressing a protein called Galectin-3. When Galectin-3 levels rise, it can damage endothelial cells and interfere with the macrophages’ energy production. Without sufficient energy, the macrophages become less effective at clearing away debris, allowing plaques to grow more rapidly.
The findings suggest that miR-147 acts as an important regulator that helps maintain a healthier balance within artery walls. By promoting cleanup activities and reducing harmful inflammation, it may help slow the progression of atherosclerosis.
The study offers an exciting possibility for future treatment. Researchers believe therapies based on miR-147 could potentially target specific inflammatory pathways inside plaques. Unlike broader anti-inflammatory treatments, this approach might preserve beneficial immune functions while reducing the harmful ones.
Study analysis: This research provides a deeper understanding of the complex role immune cells play in atherosclerosis. One major strength of the study is its use of advanced imaging technology, which allowed researchers to observe plaque development in remarkable detail.
However, the findings currently come from animal studies, meaning human studies will be necessary before any treatments can be developed. Even so, the discovery of miR-147 as a key regulator represents a promising new direction for cardiovascular research and may eventually contribute to therapies that reduce the risk of heart attack and stroke.
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Source: Ludwig Maximilian University of Munich (LMU).
