Cholesterol is a type of fat that is essential for many functions in the body, including the production of hormones and cell membranes. However, too much cholesterol in the blood can be harmful because it can attach to artery walls and form plaques that narrow or block blood flow. This causes atherosclerotic cardiovascular disease, which is the main underlying cause of heart attacks and strokes and is the leading cause of death worldwide.

the liver responded quickly

In the current study, researchers wanted to understand how different tissues in the body respond to high levels of LDL, also known as “bad cholesterol,” in the blood. To test this, they created a system that could rapidly increase cholesterol in the blood of mice.

“Essentially, we wanted to detonate a cholesterol bomb and see what happens next,” said Stephen Mullin, lead author of the study and principal investigator at the Karolinska Institutet Solna Faculty of Medicine. says. “We found that the liver responded almost immediately and removed some of the excess cholesterol.”

However, what reacted was not normal liver cells, but a type of immune cell called Kupffer cells, which are known to recognize and eat foreign and harmful substances. The findings made in mice were also validated in human tissue samples.

“We were surprised to learn that the liver is the first line of defense against excess cholesterol, and that Kupffer cells play a role in this,” says Stephen Mullin. “This shows that the liver’s immune system is actively involved in regulating cholesterol levels and that atherosclerosis is a systemic disease that affects multiple organs, not just the arteries. It suggests.”

Multiple organs may be involved

Researchers hope that by understanding how the liver and other tissues communicate with each other after exposure to high cholesterol, they can find new ways to prevent or treat cardiovascular and liver disease. ing.

“Our next steps are to examine how other organs respond to excess cholesterol and how they interact with the liver and blood vessels in atherosclerosis.” ” says Stephen Mullin. “This could help us develop more comprehensive and effective strategies to combat this common and deadly disease.”