Abstract
Aortic diseases comprise aneurysms, dissections, and several other pathologies. In general, aging is associated with a slow but progressive dilation of the aorta, along with increased stiffness and pulse pressure. The progression of aortic disease is characterized by subclinical development or acute presentation. Recent evidence suggests that inflammation participates causally in different clinical manifestations of aortic diseases. As of yet, diagnostic imaging and surveillance is mainly based on ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI). Little medical therapy is available so far to prevent or treat the majority of aortic diseases. Endovascular therapy by the introduction of covered stentgrafts provides the main treatment option, although open surgery and implantation of synthetic grafts remain necessary in many situations. Because of the risks associated with surgery, there is a need for identification of pharmaceutical targets interfering with the pathophysiology of aortic remodeling. The participation of innate immunity and inflammasome activation in different cell types is common in aortic diseases. This review will thus focus on inflammasome activities in vascular cells of different chronic and acute aortic diseases and discuss their role in development and progression. We will also identify research gaps and suggest promising therapeutic targets, which may be used for future medical interventions.
Highlights
Thoracic and abdominal aortic diseases pose a life-threatening condition affecting various congenital and acquired pathologies, either acutely or chronically
We recently demonstrated that Aim2 deficiency affects the phenotype of murine aortic vascular smooth muscle cells (VSMC), thereby reducing Angiotensin II (AngII)-induced formation of aortic aneurysm in six month old mice [53]
For both acute and chronic aortic diseases, different stimulating components have been identified, which act as pathogen associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs) on aortic cells, thereby activating specific TLRs and inflammasome receptors
Summary
Thoracic and abdominal aortic diseases pose a life-threatening condition affecting various congenital and acquired pathologies, either acutely or chronically. Recent evidence from animal models, histological analysis of human aortic tissues, and cell culture experiments propose a causative input of inflammatory mechanisms in both aortic aneurysms [5] and acute aortic syndromes [6]. Inflammation is an adaptive response of cells and tissues to different stress conditions and triggers, such as infections and tissue injury [11] It comprises two phases, innate and adaptive response, which are mediated by a coordinated process of intracellular and intercellular events. More than twenty different PRRs have been described, a subset of which have been confirmed to initiate inflammasome assembly These include nucleotide-binding oligomerization domain, leucine-rich repeatcontaining (NLR) family members NLRP1, NLRP3, NLRC4, NLRP6, NLRP7, and NLRP9b, as well as the DNA sensor proteins Absent in Melanoma 2 (AIM2), Pyrin, and IFI16 [12,13,14]. The following chapters will summarize the current knowledge on inflammasome activities in vascular (aortic) cells, infiltrating and peripheral leukocytes, and their contribution to different aortic diseases
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