Relationship between inflammatory-related cytokines with aortic dissection

Abstract

Aortic dissection, characterized by severe intramural hematoma formation and acute endometrial rupture, is caused by excessive bleeding within the aortic wall or a severe tear within the intimal layer of the aorta, which subsequently promotes the separation or dissection in the layers of the aortic wall. Epidemiological surveys showed that aortic dissection was most observed among those patients from 55 to 80 years of age, with a prevalence of approximately 40 cases per 100,000 individuals per year, posing serious risks to future health and leading to high mortality. Other risk factors of aortic dissection progression contained dyslipidemia, hypertension, and genetic disorders, such as Marfan syndrome. Currently, emerging evidence indicates the pathological progression of aortic dissection is significantly complicated, which is correlated with the aberrant infiltration of pro-inflammatory cells into the aortic wall, subsequently facilitating the apoptosis of vascular smooth muscle cells (VSMCs) and inducing the aberrant expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interferon (IF). Other pro-inflammatory-related cytokines, including the colony-stimulating factor (CSF), chemotactic factor, and growth factor (GF), played an essential function in facilitating aortic dissection. Multiple studies focused on the important relationship between pro-inflammatory cytokines and aortic dissection, which could deepen the understanding of aortic dissection and further guide the therapeutic strategies in clinical practice. The present review elucidated pro-inflammatory cytokines' functions in modulating the risk of aortic dissection are summarized. Moreover, the emerging evidence that aimed to elucidate the potential mechanisms wherebyvarious pro-inflammatory cytokines affected the pathological development of aortic dissection was also listed.

Keywords: Aortic dissection; Cytokine; Inflammation; Mechanism; Pathological development.