Atherosclerosis and aortic aneurysm – is inflammation a common denominator?

Abstract

Cardiovascular diseases (CVD) are the major cause of death in developed countries. Various risk factors including host genetics and, more importantly, environmental factors such as lifestyle, diet and smoking influence CVD progression. Two common forms of CVD are atherosclerosis and abdominal aortic aneurysm (AAA). Emerging evidence suggests that inflammation plays a pivotal role in CVD. However, it remains unclear whether the same inflammatory pathways prove essential for atherosclerosis and AAA because, in some cases, the same mechanisms uniformly promote both diseases, while in others they function in opposite ways. Cytokines, key mediators of inflammation, play an important role in the development of atherosclerosis but have only been scarcely studied in AAA. In this review, we discuss the importance of immune‐mediated mechanisms and cytokines in the pathogenesis of atherosclerosis and AAA.

Aneurysm-Specific miR-221 and miR-146a Participates in Human Thoracic and Abdominal Aortic Aneurysms

“…Aortic aneurysms occur secondary to pathologic remodeling of the aortic wall and are frequently associated with hypertension [2], atherosclerosis [3,4] in the abdominal aorta, and bicuspid aortopathy [5], or connective tissue disorders [6] in the ascending thoracic aorta. The pathogenesis of aneurysms differs based on the involved aortic segment.…”

IL-27 receptor signaling regulated stress myelopoiesis drives Abdominal Aortic Aneurysm development

“…Several cytokines have been implicated in the regulation of immune cells in AAA site 3,29,49,50,51,52,53,54,55 ; however, the possible contribution of cytokine signaling in controlling of AAAdriven "stress induced" HSCs expansion and differentiation toward myeloid lineages has never been reported. Here, we for the first time establish IL-27R signaling as a critical regulator of Ang II-driven proliferation and differentiation of HSC, essential for Ang II-induced stress myelopoiesis in a non-infectious, chronic vascular injury model.…”

“…Inactivation of IL-27R exacerbates atherosclerosis 26,27,28 and leads to the development of abdominal aortic lesions which typically are rare in atherosclerotic mice. As atherosclerosis and AAA may share some underlying chronic inflammatory mechanisms 29 , we anticipated that IL-27R-deficiency would increase inflammation and promote AAA.…”

The Association of Serum Thrombomodulin with Endothelial Injuring Factors in Abdominal Aortic Aneurysm

“…Due to the fact that the same factors participate in the atherosclerotic plaque formation, it is difficult to state whether the above observations represent a true association with AAAs or if they simply reflect the higher incidence of atherosclerotic disease found in this group of patients. Both diseases affect arteries, share predisposing risk factors, and exhibit similar immune and inflammatory cell infiltrates [57]. Moreover, one of the hypotheses assumes that AAA develops as a pathological response to aortic atherosclerosis [24].…”