Key points
- Research began with a study of more than 5,000 people without diagnosed heart disease
- Those with higher levels of suPAR were significantly more likely to develop atherosclerosis
- They developed atherosclerosis regardless of their cholesterol or blood pressure readings
ISLAMABAD: Doctors have focused on controlling high blood pressure, cholesterol and diabetes to fight heart disease for a long time.
While medications have helped many, heart disease remains the leading cause of death in the world. Now, a new discovery may explain why people still suffer heart attacks even when these risk factors are under control.
suPAR
Researchers at the University of Michigan have identified a protein, called suPAR (soluble urokinase plasminogen activator receptor), that could be a key driver of atherosclerosis—the buildup of plaque in arteries that leads to heart attacks and strokes.
Unlike cholesterol or blood pressure, suPAR is produced by the immune system and appears to directly cause damage to artery walls. The study, published in the Journal of Clinical Investigation, is the first to show that suPAR may be a direct cause of atherosclerosis, not just a marker of inflammation.
The research began with a study of more than 5,000 people without diagnosed heart disease. Those with higher levels of suPAR were significantly more likely to develop atherosclerosis, regardless of their cholesterol or blood pressure readings.
Genetic data
To understand why suPAR levels vary, the team examined genetic data from 24,000 people and found a variant in the PLAUR gene, which produces suPAR. People with this genetic variant had both higher suPAR levels and a higher risk of developing atherosclerosis.
Using a method called Mendelian randomisation—analysing genetic information to determine cause-and-effect—the researchers confirmed their findings in more than 500,000 participants from the UK Biobank and two other large datasets.
The team also tested their theory in mice. Animals given high levels of suPAR developed more plaque in their aortas than those with normal levels, providing further evidence that suPAR contributes directly to artery damage.
