Scientists from Lund University in Sweden have made a surprising discovery about how aging blood vessels respond to stress.
By simulating aging in mice, they were able to closely watch how weak spots, called aneurysms, form in the walls of blood vessels. These findings, published in the Journal of Biological Chemistry, could one day lead to new kinds of blood pressure medicine.
In Sweden, about one in five people has high blood pressure. As people get older, their blood vessels become stiffer and more vulnerable to damage.
This stiffness can increase blood pressure and, in some cases, lead to serious conditions like aortic aneurysms. An aneurysm is when a blood vessel wall weakens and starts to bulge, which can be life-threatening if it bursts.
To better understand this process, researchers focused on a protein called serum response factor (SRF). SRF helps control which genes are active in the smooth muscle cells that make up the blood vessel walls.
The scientists removed this protein in mice to mimic how blood vessels age. As expected, the mice quickly began to show early signs of aneurysms.
However, what happened next surprised the researchers. Even though the vessels were becoming weaker, the mice were somehow protected from high blood pressure.
This protection seemed to come from another set of proteins called YAP/TAZ, which are also known to decline with age. When SRF was removed, YAP/TAZ became more active. The scientists believe this may be the body’s way of trying to protect the vessel wall.
This interaction appears to be controlled by an enzyme called LATS2. Normally, LATS2 shuts down YAP/TAZ. But when SRF levels go down, LATS2 also drops, allowing YAP/TAZ to step in and help.
Professor Karl Swärd from Lund University compared it to classical music. He called SRF the “Mozart” of blood vessels—a master composer keeping everything in order. When Mozart becomes less active, “Beethoven,” or YAP/TAZ, steps in to help.
In earlier research, the team also showed that when YAP/TAZ was removed in mice, the vessel walls were quickly damaged, leading to aneurysms. Instead of staying as muscle cells, the cells began turning into cartilage-like cells, causing scarring and inflammation.
Now, the researchers are excited by the possibility that adjusting the activity of LATS2 could protect blood vessels. Most drugs that block LATS2 also block a related enzyme called LATS1, which could lead to unwanted side effects.
So the team’s next step is to figure out which version of LATS2 exists in the blood vessels and develop a way to block only that one.
In the future, the goal is to create a genetic knockout that targets LATS2 in the blood vessels specifically. This could provide protection against damage caused by high blood pressure and offer a new way to treat people with vascular problems.
Although creating such a treatment could take years, the researchers are optimistic. They’ve already found that activating SRF increases LATS2 nearly 200 times. These results give important clues about how blood vessels adjust to the constant pressure of blood flow and may lead to better ways to protect them as we age.
If you care about high blood pressure, please read studies that early time-restricted eating could help improve blood pressure, and natural coconut sugar could help reduce blood pressure and artery stiffness.
For more health information, please see recent studies about added sugar in your diet linked to higher blood pressure, and results showing vitamin D could improve blood pressure in people with diabetes.
Copyright © 2025 Knowridge Science Report. All rights reserved.
