Cellular Senescence and Abdominal Aortic Aneurysm
In recent years, researchers have presented evidence for the age-related accumulation of senescent cells to be a meaningful contributing cause of aneurysm, the formation of a bulging weak spot in a blood vessel, vulnerable to bursting. Relatedly, pro-inflammatory immune cells are also implicated. The commonality here is inflammatory signaling, disruptive to tissue function. Here researchers review the mechanisms likely involved, and the high points of existing evidence for a relationship between the presence of senescent cells and formation of aneurysms.
Abdominal aortic aneurysm (AAA) is locally weak and aneurysm-like dilatation of the abdominal aorta, with a diameter of 3 cm or more, more than 1.5 times the normal diameter AAA is a common disease among the elderly, and the incidence of AAA increases with age. Most AAA patients are asymptomatic and are discovered accidentally during a physical exam or ultrasound screening. However, rupture or precursor rupture may occur when patients present with symptoms such as lumbago and abdominal pain. The in-hospital mortality rate of rupture is about 40%, while the out-of-hospital mortality rate can be as high as 90%, resulting in about 150,000-200,000 deaths globally per year.
The threat of AAA mainly in elderly patients is becoming more and more serious. Currently there is no effective method to inhibit AAA progress via treatment with clinical drug. Thus it is of great clinical significance to study the pathogenesis of AAA and explore potential therapeutic targets. The purpose of this paper is to analyze the pathogenesis of AAA from the perspective of cellular senescence: on the basis of clear evidence of cellular senescence in aneurysm wall, we actively elucidate specific molecular and regulatory pathways, and to explore the targeted drugs related to senescence and senescent cell elimination measures, eventually improve the health of patients with AAA and prolong the life of human beings.