Wang Xinhao, Zhang Hongpeng, Cao Long, He Yuan, Ma Airong, Guo Wei
Department of Vascular and Endovascular Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, China.
Department of General Surgery, PLA No. 983 Hospital, Tianjin, China.
Front Physiol. 2020 Feb 5;11:54. doi: 10.3389/fphys.2020.00054. eCollection 2020.
Aortic dissection (AD) is a fatal disease that accounts for a large proportion of aortic-related deaths and has an incidence of about 3-4 per 100,000 individuals every year. Recent studies have found that inflammation plays an important role in the development of AD, and that macrophages are the hub of inflammation in the aortic wall. Aortic samples from AD patients reveal a large amount of macrophage infiltration. The sites of macrophage infiltration and activity vary throughout the different stages of AD, with involvement even in the tissue repair phase of AD. Angiotensin II has been shown to be an important factor in the stimulation of macrophage activity. Stimulated macrophages can secrete metalloproteinases, inflammatory factors and other substances to cause matrix destruction, smooth muscle cell apoptosis, neovascularization and more, all of which destroy the aortic wall structure. At the same time, there are a number of factors that regulate macrophages to reduce the formation of AD and induce the repair of torn aortic tissues. The aim of this review is to take a close look at the roles of macrophages throughout the course of AD disease.
主动脉夹层(AD)是一种致命疾病,在与主动脉相关的死亡中占很大比例,每年发病率约为每10万人中有3 - 4例。最近的研究发现,炎症在AD的发展中起重要作用,巨噬细胞是主动脉壁炎症的中心。AD患者的主动脉样本显示有大量巨噬细胞浸润。巨噬细胞浸润和活动的部位在AD的不同阶段各不相同,甚至在AD的组织修复阶段也有涉及。血管紧张素II已被证明是刺激巨噬细胞活性的一个重要因素。被激活的巨噬细胞可分泌金属蛋白酶、炎症因子等物质,导致基质破坏、平滑肌细胞凋亡、新生血管形成等,所有这些都会破坏主动脉壁结构。同时,有许多因素调节巨噬细胞以减少AD的形成并诱导撕裂的主动脉组织修复。这篇综述的目的是深入探讨巨噬细胞在AD病程中的作用。