SAN FRANCISCO — Researchers at the University of California, San Francisco published a study on aneurysm biology in the journal Nature Neuroscience on June 10, 2026. The study revealed cellular mechanisms connected to the formation and rupture of brain aneurysms.
Scientists analyzed more than 100,000 individual cells from human aneurysm samples and healthy brain arteries. This cellular analysis identified 19 distinct cell types and mapped their organization within the blood vessel wall.
Healthy brain arteries consist of a thin inner lining, a thick middle layer of smooth muscle, and an outer layer of fibroblasts. In aneurysm tissue, the arterial layers become disorganized, and smooth muscle cells frequently disappear. Scar-forming cells known as activated fibroblasts replace the lost smooth muscle cells in aneurysm tissue.
Activated fibroblasts stiffen the arterial wall and reduce its ability to flex. These cells also express genes associated with an inherited risk of aneurysms. A specific type of immune cell, called a macrophage, accumulates inside the arterial wall near activated fibroblasts.
These macrophages express a gene typically associated with bone tissue. Activated fibroblasts release a chemical signal that triggers nearby macrophages to produce enzymes, which degrade the blood vessel's structural support. Experimental blocking of this fibroblast signal reduced the production of vessel-degrading enzymes by macrophages.
Approximately one in fifty Americans has a brain aneurysm, which are bulges in blood vessels that can remain asymptomatic for years. The rupture of a brain aneurysm can cause a severe type of stroke. Clinical decisions for treatment typically rely on the aneurysm's size, location, and patient-specific risk factors. Aneurysms measuring less than seven millimeters are generally monitored rather than surgically repaired.
Dr. Ethan Winkler, an assistant professor of Neurological Surgery, observed that more than half of the aneurysm ruptures he treated early in his career occurred in aneurysms below the seven-millimeter surgical threshold. The biological process of vessel wall weakening explains why aneurysms smaller than seven millimeters can still rupture. "We've made major steps toward solving the mystery of how aneurysms form," Winkler said. "We've identified the cast of characters involved and seen which ones are implicated at different phases of disease," he said.
No independent assessment of UC San Francisco’s claims was available.