Scientists at the Stanford Institute of Cardiovascular Diseases have found that cholesterol-lowering drugs also improve blood vessel health by changing the activity of genes in cells in the vessel wall. The research was published in the journal Nature Cardiovascular Research.
Statins are drugs developed in the 1980s from compounds found in molds and fungi. They bind to an enzyme that regulates cholesterol production in the liver. But clinical trials have shown that statins protect against cardiovascular disease through other mechanisms besides their ability to lower cholesterol levels.
For example, heart failure patients who take statins are less likely to have another heart attack. It has also been shown to prevent clogged arteries, reduce inflammation and even reduce the risk of cancer. However, the mechanisms underlying these effects are not fully understood.
To better understand the effect of statins on blood vessels, the scientists tested a statin drug, simvastatin, on human endothelial cells grown in the lab. Endothelial cells line the blood vessels from the inside, but in many diseases they turn into another cell type – mesenchymal. This makes the veins more rigid: they cannot relax or contract properly.
The researchers suspected that statins might reduce this harmful transition from endothelial cells to mesenchymal cells. Scientists have confirmed this hypothesis. This effect has been associated with a decrease in the activity of genes that cause endothelial-mesenchymal transition. Interestingly, the change in gene activity resulted from a change in DNA packaging in cells.
The scientists also tested simvastatin in diabetic mice. They found that after eight weeks of taking simvastatin, the diabetic mice had significantly improved vascular function, with arteries relaxing and contracting better.
“If we can understand the mechanism, we can modify simvastatin to further improve vascular function,” the authors explained.