On Apr. 3, 2025, a Stanford-led study has found that the gene CXCL12 is connected to the posterior descending artery formation and that its directional pattern is set very early in human development.

Most people have right-dominant hearts – which to a doctor or a researcher means they have an artery that extends from the right side of their hearts to supply oxygenated blood to the back side. For some people, this artery, the posterior descending artery, comes from the left side or from both directions.

For an estimated 80% of humans, that artery comes from the right main coronary artery, but for about 10%, it comes from the left. In another 10%, there are two of these arteries of roughly equal size that branch off the right and left main arteries and extend to the back of the heart.

The findings, reported in the journal Cell, represent a step toward developing “medical revascularization,” a long-term goal of Stanford researchers to create a treatment for blocked or limited-flow arteries by growing new ones to compensate.

“For the first time, we have evidence of a gene that regulates the development of one of the most important types of arteries in the human body,” said Kristy Red-Horse, co-senior author of the study and biology professor in the Stanford School of Humanities and Sciences. “And if we know the development pathways of these important arteries, then we can perhaps regrow them by reintroducing these pathways in a diseased heart.”

The discovery of the gene that potentially controls this branching opens up the possibility of discovering ways to make new collateral arterial branches, meaning purposefully growing additional arteries that could still deliver oxygen to the heart when another artery is blocked. Currently, treatments to relieve limited or blocked arteries are invasive and mechanical, such as open-heart bypass surgery and the placement of artificial stents.

Next the researchers plan to investigate the DNA variants that cause differences in expression of CXCL12 and work on designing ways to target the gene activation toward the creation of a therapeutic treatment.