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脂联素和血管周脂肪组织在腹主动脉瘤中的作用:动物和人体观察性研究的系统评价和荟萃分析。

Role of Adipokines and Perivascular Adipose Tissue in Abdominal Aortic Aneurysm: A Systematic Review and Meta-Analysis of Animal and Human Observational Studies.

机构信息

The Queensland Research Centre for Peripheral Vascular Disease (QRC-PVD), College of Medicine and Dentistry, James Cook University, Townsville, QLD, Australia.

The Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, QLD, Australia.

出版信息

Front Endocrinol (Lausanne). 2021 Mar 15;12:618434. doi: 10.3389/fendo.2021.618434. eCollection 2021.

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.

摘要

需要更好地了解腹主动脉瘤(AAA)的发病机制,以确定治疗靶点。本系统综述总结了来自动物研究和临床研究的证据,这些研究检查了脂肪因子和血管周围脂肪组织(PVAT)在 AAA 发病机制中的作用。荟萃分析表明,在动物模型中,瘦素(标准化均数差 [SMD]:0.50 [95%置信区间(CI):-1.62,2.61])和脂联素(SMD:-3.16 [95% CI:-7.59,1.28])的上调并未显著影响 AAA 的严重程度。有研究表明抵抗素样分子-β(RELMβ)和 PVAT 在 AAA 动物模型中的作用存在不一致的发现和有限的研究。临床研究表明,与对照组相比,诊断为 AAA 的患者循环瘦素(SMD:0.32 [95% CI:0.19,0.45])和抵抗素(SMD:0.63 [95% CI 0.50,0.76])浓度以及 PVAT 与腹部脂肪组织的比值(SMD:0.56 [95% CI 0.33,0.79])显著更高。血清脂联素水平与 AAA 诊断无关(SMD:-0.62 [95% CI -1.76,0.52])。一项、八项和一项动物研究以及两项、两项和四项人类研究的偏倚风险分别为低、中和高。这些发现表明,与对照组相比,AAA 与更高的循环瘦素和抵抗素浓度以及更多的 PVAT 相关,但这是否在动脉瘤发病机制中起作用尚不清楚。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e26/8008472/07955f7d464f/fendo-12-618434-g001.jpg

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