Researchers at UCLA Health announced on May 14 that they have identified a gene, MYH9, which may help explain why women are more likely than men to develop a specific type of artery plaque associated with heart disease. The study, published in Circulation Research and led by Dr. Mete Civelek at the David Geffen School of Medicine at UCLA, highlights differences in how heart disease develops between women and men.
This research matters because it sheds light on biological mechanisms behind sex-specific risks for cardiovascular disease. Heart disease is the leading cause of death among women worldwide, yet its symptoms are often overlooked or misdiagnosed due to differences from typical male presentations.
“Although heart disease is the No. 1 killer of women worldwide, taking more women’s lives than all forms of cancer combined, it’s often over looked or misdiagnosed because symptoms and imaging may not ‘look like’ what we typically see in men’s heart disease,” said Dr. Mete Civelek. “We’ve known that women and men can develop different kinds of plaques in their arteries, but the underlying biology has remained a mystery, which is why we wanted to look more closely at the specific cells that help build and stabilize plaques.”
The international team analyzed vascular smooth muscle cells from over 150 human donors—119 males and 32 females—and found female-specific gene networks tied to inflammation and cell structure changes. They discovered two female-biased “gene programs,” one strongly involving MYH9. Higher levels of this gene were linked to fibrous plaques containing more smooth muscle cells and less fat—features considered generally more stable but still risky due to potential erosion.
Civelek explained: “Using a variety of advanced analytical and computational methods, we compared cells from women and men and looked at how groups of genes work together.” He added that large human cohort studies from the Netherlands and Sweden supported their findings.
The study suggests MYH9 could influence how vascular cells respond differently in men versus women when exposed to stress or hormones—a factor potentially shaping plaque development based on sex-specific biology.
Civelek said these results will not change patient care immediately but offer better understanding for future personalized treatments: “In the long run,” he said, “findings like ours will help to develop more personalized ways to predict risk and design treatments that take sex differences into account.” Further collaboration is underway with Dr. Karen Reue’s lab at UCLA focusing on whether sex hormones or chromosomes drive these observed differences.
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