Smooth Muscle Cells in Blood Vessel Stiffening

Blood vessels lose their flexibility and structural integrity with age, which contributes to a range of ultimately fatal cardiovascular conditions, as well as loss of cognitive function caused by disruption of blood flow in the brain. This process of stiffening in blood vessels is thought to be at least partially due to cross-linking in the extracellular matrix, in which the mechanical properties of tissue degrade due to rising levels of advanced glycation endproducts, sugary metabolic wastes that can glue together proteins to disrupt their function.

Here, however, researchers look at another potential causative process for vascular stiffness, in this case connected to focal adhesion structures. These are built by cells in order to anchor to the extracellular matrix and hold steady in its tissue, but can be quite dynamic in some circumstances, destroyed and recreated as a cell shifts its position:

The aorta is the main artery of the body. It is connected to the heart and carries oxygen-rich blood pumped from the left ventricle to the rest of the circulatory system. Pumping blood from the heart causes pulsing waves that reverberate into the aorta. As it branches off into smaller blood vessels, the aorta acts as a shock absorber, blunting the impact of these waves. But with age, changes in the blood vessel wall can cause the aorta to lose some of its flexibility and its ability to buffer high-pressure waves as they travel to the smaller vessels. The reduced shock-absorbing capacity can lead to changes in microcirculations and negative effects on organ function.

The underlying cause of aortic stiffening is unclear. While much of the previous research pointed to the extracellular matrix (ECM) - a group of molecules secreted by the cells that support cell attachment and communication - as the culprit, a few studies suggest that vascular smooth muscle may play a role. [Researchers] directly measured the mechanical properties of the aortas of young and old mice to observe how smooth muscle cells factor into aortic wall stiffness. They also observed how focal adhesion signaling - which helps promote arterial flexibility in young mice - is impaired with aging. They used a novel biomechanical method to distend the aorta, mimicking circumferential strain, to measure how the smooth muscle affected arterial stiffness.

"A major finding of the present study is that the smooth muscle cell is a major source and regulator of vascular stiffness, in contrast with the often-assumed dominance of ECM in effecting changes in wall stiffness with aging. The decrease in the focal adhesion signaling mechanism led to higher stiffness in old vessels. We conclude from our results that the smooth muscle focal adhesions represent a potential therapeutic target in the context of preventing or reversing increases in aortic stiffness. An understanding of this mechanism may lead to an approach to reverse this aging-induced deficiency."


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