Blood-cell mutation worsened aortic aneurysms in mice
After bone marrow transplantation and four weeks of hormone infusion, mice with an Asxl1 mutation developed more aneurysms and ruptures than controls.
Limit: The abstract gave no sample sizes or numerical effect sizes
Edited by Boris Djordjevic · AgingResearch.News
In an animal experiment, genetically modified mice received bone marrow with or without a mutation in Asxl1, a gene that helps control gene activity. Researchers then infused the mice with angiotensin II, a hormone, for four weeks and measured the abdominal aorta, the main artery carrying blood through the abdomen.
Mice with the mutation developed more aneurysms, bulges in the artery wall, and more ruptures than controls. They also accumulated more macrophages, immune cells involved in inflammation, around the artery. Macrophages grown in the lab showed greater activation of the NLRP3 inflammasome, a protein complex involved in inflammation, when they carried the mutation. Colchicine suppressed this activity in the cells. In mice, the drug reduced aneurysm formation, rupture and macrophage accumulation.
Why it matters
Age-associated expansion of mutated blood cells is linked to cardiovascular disease. The work suggests that targeting inflammation may offer a way to limit aneurysm progression in this setting.
Caveats
The findings came from a genetically modified, bone-marrow-transplanted mouse model and lab-grown cells, not people. This congress abstract gave no sample sizes, colchicine doses or numerical effect sizes.
The paper
The University of Tokyo Hospital; Kanazawa Medical University
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
