New ways to dismantle a ticking time bomb: MicroRNA 712/205 and abdominal aortic aneurysm development

摘要

Abdominal aortic aneurysms (AAAs) are permanent dilations (>3 cm) of the abdominal aorta that are typically asymptomatic, and the discovery of these potentially deadly vascular lesions is almost always incidental. The most feared clinical consequence of AAA progression is acute rupture, which carries a mortality of 80%, and the number of deaths attributed to AAA rupture is ?15 000 annually in the United States.1 However, this number is likely an underestimate because death from AAA rupture may not be readily identified without an autopsy. Sixty percent of patients with AAAs die of other cardiovascular causes, such as myocardial infarction or stroke, suggesting a relationship between AAAs and atherosclerosis. Predictors of AAA growth include diameter of the aorta at diagnosis, advanced age (>65 years), and active smoking.2 Currently, the only available effective treatment option is surgical repair, either via the traditional open approach or, more commonly, endovascular stenting. Furthermore, neither procedure is used in the early stages of the disease, and both carry potential operative risks. Although AAA disease is a common cause of morbidity and mortality in our aging society, it remains a somewhat understudied disease, with a paucity of information available regarding defined mechanisms of initiation and expansion. Importantly, no pharmacological treatment option has been found to prevent the formation of AAAs or effectively slow the growth of these ticking time bombs.