The role of histone modifications in the development of abdominal aortic aneurysm.

Cardiovascular diseases with their related secondary complications are the main causes of morbidity and mortality worldwide. Abdominal aortic aneurysm (AAA) belongs to the cardiovascular diseases and causes approximately 1.3 % of all deaths among men between 65 and 85 years old in developed countries [1]. The pathogenesis of AAA mainly attributes to pathological dilation of the abdominal aorta, which will further lead to a high mortality rate up to 85 % due to excessive dilation and rupture [2]. A criterion was proposed in 1991 that AAA infrarenal aorta diameter should be 1.5 times the normal diameter [3], and McGregor additionally defined AAA as an aorta with a diameter greater than 30 mm in the infrarenal segment [4]. Although the diagnosis of AAA seems conclusive, there is no specific treatment to prevent AAA expansion. Elective aortic repair operation is conditional recommended when the aneurysm diameter reaches 55 mm in men, 50 mm in women or grows by 6 mm to 8 mm per year [5]. However, small aneurysms probably also grow rapidly or rupture at a high risk, and even some patients die from aneurysm rupture before they manifest surgical indications. Thus, controlling risk factors and exploring novel therapeutic approaches gradually substitute as key directions for aneurysm treatment. Smoking, hypertension, age and gender have been identified as the common risk factors during AAA progression in the past decades [6], but the mechanisms how these hazards contribute to pathological dilatation of abdominal aortas remain unclear. Interestingly, histone modifications have recently emerged as an important link between the intrinsic genetic landscape and extrinsic risk factors, and a plethora of studies have been dedicated to exploring the role of histone modifications in AAA pathogenesis. In this review, current progress on the contribution of histone modifications to the regulation of AAA will be summarized.