High blood pressure, or hypertension, is a major risk factor for heart attacks and strokes. It happens when the force of blood pushing against your artery walls stays too high for too long.
Over time, this pressure changes the structure of the blood vessels, a process called vascular remodeling. These changes make the arteries stiffer and narrower, raising the risk of serious health problems.
Now, researchers at Michigan Medicine have discovered a key piece of the puzzle that explains how a common genetic trait affects blood pressure—and how it might be treated in the future.
Their study, published in The Journal of Clinical Investigation, looked closely at the role of a protein called JMJD3 and how it interacts with a well-known blood pressure pathway in the body.
JMJD3 is an enzyme that controls how certain genes are turned on or off. It’s been linked to blood pressure in large genetic studies. The researchers found that JMJD3 has a direct effect on how blood vessels behave by regulating two types of receptors (called endothelin receptors) on smooth muscle cells in the artery walls.
These receptors control whether blood vessels tighten (constrict) or relax (dilate). When JMJD3 levels were lowered in mice, the balance between these receptors shifted.
There was less of the “relaxing” receptor (endothelin receptor-B) and more of the “tightening” receptor (endothelin receptor-A). This change made the blood vessels constrict more than they should, which raised blood pressure and triggered long-term damage to the arteries.
This process is especially important for people with a common genetic variant called rs62059712. About 90% of people carry the T version of this gene, which the researchers found reduces the amount of JMJD3 made in the body.
That means these individuals are more likely to have overactive blood vessel constriction and more long-term artery damage—putting them at greater risk for high blood pressure, heart disease, and stroke.
But there’s hope. In the same study, researchers were able to reverse high blood pressure in mice lacking JMJD3 by using a drug that blocks the endothelin receptor-A. The drug, called BQ-123, helped relax the blood vessels and bring blood pressure back down. This suggests that people with the rs62059712 variant could benefit from a treatment that targets this specific receptor.
Dr. Katherine Gallagher, senior author of the study, says this kind of targeted approach could offer personalized therapy for people who are genetically at risk. “Instead of a one-size-fits-all treatment, we can design therapies that work best for people based on their individual genetic profiles,” she explained.
The researchers believe that their method of studying JMJD3 and its effects could be used to better understand many other genetic variants linked to heart disease. With more studies like this, it might become possible to match patients with treatments that are customized to their unique DNA.
In short, this discovery could open the door to new ways of managing high blood pressure—especially for the many people whose genes put them at greater risk. It’s another step forward in using science to bring more precise, effective treatments to those who need them most.
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The research findings can be found in The Journal of Clinical Investigation.
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