Relationships Between Perivascular Adipose Tissue and Abdominal Aortic Aneurysms

Abstract

Abdominal aortic aneurysms (AAAs) are typically asymptomatic, and there is a high mortality rate associated with aneurysm rupture. AAA pathogenesis involves extracellular matrix degradation, vascular smooth muscle cell phenotype switching, inflammation, and oxidative stress. There is increasing evidence of excessive adipocyte accumulation in ruptured AAA walls. These excessive numbers of adipocytes in the vascular wall have been closely linked with AAA progression. Perivascular adipose tissue (PVAT), a unique type of adipose tissue, can be involved in adipocyte accumulation in the AAA wall. PVAT produces various chemokines and adipocytokines around vessels to maintain vascular homeostasis through paracrine and autocrine mechanisms in normal physiological conditions. Nevertheless, PVAT loses its normal function and promotes the progression of vascular diseases in pathological conditions. There is evidence of significantly reduced AAA diameter in vessel walls of removed PVAT. There is a need to highlight the critical roles of cytokines, cells, and microRNA derived from PVAT in the regulation of AAA development. PVAT may constitute an important therapeutic target for the prevention and treatment of AAAs. In this review, we discuss the relationship between PVAT and AAA development; we also highlight the potential for PVAT-derived factors to serve as a therapeutic target in the treatment of AAAs.

Immune and inflammatory mechanisms of abdominal aortic aneurysm

“…It is infiltrated by multiple immune cells ( 234 ) and heavily innervated ( 246 , 247 ). In pro-inflammatory environment or under the conditions of lipid overload, adipocytes become activated and produce pro-inflammatory cytokines (including TNF and IL-6) and adipokines (such as leptin) which further facilitate immune and VSMC cell activation ( 234 , 248 – 250 ). Increased adiposity and lipid deposition is associated with the shift toward white adipocytes and heightened accumulation of pro-inflammatory immune cell types ( 251 ), for example pro-inflammatory adipose macrophages ( 252 ).…”

EGR1 and KLF4 as Diagnostic Markers for Abdominal Aortic Aneurysm and Associated With Immune Infiltration

“…During the AAA formation and progression, the three-layered vascular wall of the abdominal aorta gradually expands and weakens ( 4 ). Inflammatory cell infiltration, oxidative stress, vascular smooth muscle cell (VSMC) depletion, and destructive extracellular matrix are the primary pathophysiology mechanism of AAA ( 5 , 6 ).…”

“…Perivascular adipose tissue (PVAT) is a unique tissue in organism and initially thought to provide mechanical support for the vessel wall, which surrounds most blood vessels including the abdominal aorta ( 5 , 11 ). Multicenter research showed differences in PVAT distribution for patients with AAA.…”

“…A more recent study has demonstrated that the pathogenesis of AAA was associated with immune cells from PVAT ( 5 ). There was immune cell infiltration in the lesion of AAA.…”

“…T cells are the most important component, and B cells, macrophages, and NK cells also account for a proportion ( 17 ). Noteworthy, with the diameter of AAA increased, the degree of immune cell infiltration in the PVAT and abdominal aorta wall was concomitant elevated ( 5 , 18 ). In addition, artery tertiary lymphoid organs (ATLOs) and pericardial adipose tissue have a regulatory effect on the accumulation of immune cells ( 19 , 20 ).…”