Aneurysms are the abnormal enlargement of arteries and can lead to death if the artery wall bursts. Oller et al. studied patients with Marfan syndrome, an inherited genetic condition in which individuals are prone to cardiac aneurysms. They discovered lower levels of ADAMTS1 in the heart tissue of Marfan syndrome patients compared with that of organ transplant donors. Genetic inactivation of ADAMTS1 in mice resulted in a Marfan syndrome-like disease, which included low blood pressure, aortic dilation, and aneurysm development. These effects were driven by enhanced activity of nitric oxide, and treatment with a nitric oxide inhibitor reduced blood vessel size and reversed the clinical signs of aneurysm formation.
