Cardiovascular disease remains the world’s biggest killer, responsible for millions of deaths every year. Most heart attacks and strokes can be traced back to a slow-moving process that begins decades before symptoms appear.
This process, known as atherosclerosis, causes fatty deposits to build up inside arteries, gradually reducing blood flow and increasing the risk of sudden blockages.
Scientists have spent decades studying how these plaques develop. While cholesterol has received much of the attention, researchers now understand that the immune system is deeply involved in every stage of the disease.
A new study from Ludwig Maximilian University of Munich has revealed an unexpected player that may help control plaque growth and reduce damage inside blood vessels.
The research focused on macrophages, specialized immune cells that act like garbage collectors within the body. Their job is to find and remove harmful substances, dead cells, and other unwanted material. In healthy tissues, this process helps maintain balance and supports healing.
Inside atherosclerotic plaques, however, macrophages face a much more difficult task. They encounter large amounts of cholesterol and cellular debris. As they consume more fat, many macrophages eventually become overloaded and die. Their remains contribute to plaque growth and instability.
One particularly dangerous consequence is the formation of cholesterol crystals. These sharp crystals can make plaques more fragile and increase the likelihood that they will rupture. When a plaque ruptures, a blood clot can quickly form and block blood flow, triggering a heart attack or stroke.
To better understand these processes, the LMU researchers used sophisticated imaging techniques that allowed them to track cells inside plaques over time. Their observations revealed that not all macrophages behave the same way.
The team identified an important group of macrophages that remain relatively free of fat accumulation. These lipid-free macrophages turned out to have a surprisingly complex role.
First, they perform an important cleanup function. They remove DNA and other cellular debris left behind by dying cells. This process helps prevent the buildup of material that can contribute to cholesterol crystal formation.
At the same time, these macrophages can also cause harm. The researchers found that they sometimes attack endothelial cells, which form the protective inner lining of blood vessels. Damage to this lining may worsen vascular disease and promote inflammation.
This dual behavior demonstrates that inflammation is not simply good or bad. Instead, inflammation involves a delicate balance between protective and damaging processes. Understanding this balance is one of the biggest challenges in cardiovascular research.
The scientists discovered that a small molecule called miR-147 plays a central role in controlling these macrophages. MiR-147 belongs to a family of molecules known as microRNAs, which help regulate gene activity.
Although microRNAs are tiny, they can influence the behavior of entire cell populations. In this study, miR-147 appeared to help macrophages clear away harmful debris while limiting the damage they caused to blood vessels.
When researchers eliminated miR-147, plaque development accelerated significantly. The arteries contained more cholesterol crystals, more DNA debris, and larger plaques overall. These findings suggest that miR-147 normally acts as a protective factor within diseased arteries.
The researchers also uncovered the biological mechanism behind this effect. MiR-147 suppresses production of a protein called Galectin-3. When Galectin-3 levels rise, endothelial damage increases and macrophages lose some of their ability to generate energy efficiently.
Without adequate energy, the cells become less effective at cleaning up debris. As a result, more harmful material accumulates inside plaques, promoting disease progression.
The discovery may have important therapeutic implications. Current treatments for atherosclerosis mainly focus on reducing cholesterol levels, controlling blood pressure, and preventing blood clots. While these approaches save many lives, they do not directly address all aspects of plaque inflammation.
A future therapy based on miR-147 could potentially target specific immune processes involved in plaque growth. Such a treatment might complement existing therapies and provide additional protection against cardiovascular events.
Researchers caution that much more work is needed before this becomes a reality. The findings must first be confirmed in human studies, and scientists will need to determine whether manipulating miR-147 can be done safely and effectively.
Study analysis: This study highlights how modern cardiovascular research is moving beyond cholesterol alone and examining the immune system’s role in artery disease.
The identification of miR-147 provides a new biological target that may help researchers develop more precise treatments. While the results are preliminary and based on animal models, the work offers valuable insights into plaque biology and opens a potentially promising pathway for reducing heart attack and stroke risk in the future.
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Source: Ludwig Maximilian University of Munich (LMU).
