Abstract

Improved understanding of abdominal aortic aneurysms (AAA) pathogenesis is required to identify treatment targets. This systematic review summarized evidence from animal studies and clinical research examining the role of adipokines and perivascular adipose tissue (PVAT) in AAA pathogenesis. Meta-analyses suggested that leptin (Standardized mean difference [SMD]: 0.50 [95% confidence interval (CI): −1.62, 2.61]) and adiponectin (SMD: −3.16 [95% CI: −7.59, 1.28]) upregulation did not significantly affect AAA severity within animal models. There were inconsistent findings and limited studies investigating the effect of resistin-like molecule-beta (RELMβ) and PVAT in animal models of AAA. Clinical studies suggested that circulating leptin (SMD: 0.32 [95% CI: 0.19, 0.45]) and resistin (SMD: 0.63 [95% CI 0.50, 0.76]) concentrations and PVAT to abdominal adipose tissue ratio (SMD: 0.56 [95% CI 0.33, 0.79]) were significantly greater in people diagnosed with AAA compared to controls. Serum adiponectin levels were not associated with AAA diagnosis (SMD: −0.62 [95% CI −1.76, 0.52]). One, eight, and one animal studies and two, two, and four human studies had low, moderate, and high risk-of-bias respectively. These findings suggest that AAA is associated with higher circulating concentrations of leptin and resistin and greater amounts of PVAT than controls but whether this plays a role in aneurysm pathogenesis is unclear.

Highlights

  • Screening studies suggest that abdominal aortic aneurysms (AAA) prevalence is approximately 3% in men and 1% in women aged over 65 years (1)

  • Ten eligible rodent studies were identified (19–28). These studies included a total of 319 rodents in which the effects of leptin, resistin, adiponectin, and perivascular adipose tissue (PVAT) were investigated (19–28)

  • Animal Studies Investigating the Effect of Leptin in AAA Four studies including 159 animals investigated the role of leptin in AAA pathogenesis within mouse model induced using Angiotensin-II (Ang-II) infusion (19, 21, 22) or peri-aortic calcium chloride (CaCl2) application (20) (Table 1A)

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Summary

Introduction

Screening studies suggest that abdominal aortic aneurysms (AAA) prevalence is approximately 3% in men and 1% in women aged over 65 years (1). The main complication of AAA is aortic rupture which is estimated to cause 200,000 deaths worldwide each year (2). The management of AAA is limited to surgical repair (3). Randomized clinical trials have demonstrated that early elective surgical repair does not reduce mortality for people with small asymptomatic AAAs (4, 5). Current guidelines recommend monitoring small (

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