Researchers at a leading cardiovascular science institute have found that cholesterol-lowering drugs can boost blood vessel health by altering how genes are turned on and off in the cells that line the vessel walls. The findings were published in Nature Cardiovascular Research.
Statins, first developed in the 1980s from compounds found in molds and fungi, work by binding to an enzyme that controls cholesterol production in the liver. Yet clinical studies have shown that statins provide protective effects against heart disease through additional pathways beyond simply lowering cholesterol.
For instance, patients with heart failure who use statins appear to experience fewer recurrent heart events. Research has also indicated benefits in preventing artery blockages, dampening inflammation, and even lowering cancer risk. The exact biological mechanisms behind these additional benefits remain under investigation.
To deepen understanding, scientists examined the impact of simvastatin on human endothelial cells grown in the laboratory. Endothelial cells line the interior surface of blood vessels. In various diseases, these cells can transform into mesenchymal-like cells, a change that makes veins stiffer and less able to relax or contract properly.
The team hypothesized that statins might slow this endothelial-to-mesenchymal transition. Experiments confirmed this idea. The observed decrease in the activity of genes driving the transition aligned with changes in how DNA is packaged in the cells, suggesting a genome-wide reshaping effect tied to statin exposure.
Further work involved testing simvastatin in diabetic mice. After eight weeks of treatment, the diabetic animals showed clearer improvements in vascular function, with arteries demonstrating better relaxation and responsiveness. These functional gains point to meaningful vascular benefits beyond cholesterol reduction.
The researchers emphasized that uncovering the specific mechanism could lead to refined statin strategies. By understanding how simvastatin modulates vascular dynamics at the molecular level, scientists may design targeted approaches to maximize vascular health in patients at risk for cardiovascular complications.
Overall, the study reinforces the idea that statins influence vascular biology through multiple avenues. The evidence suggests that these drugs can modulate gene activity and chromosome structure in vessel cells, contributing to improved vessel function. Ongoing studies aim to translate these insights into optimized therapies that protect the heart and blood vessels in diverse patient populations.