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Abstract
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.
Highlights
Aortic dissection (AD) is a fatal disease that accounts for a large proportion of aortic-related deaths (Hiratzka et al, 2010)
The main histological finding related to arterial wall weakening in AD is medial degeneration, which consists of profound degradation of the extracellular matrix (ECM) involving smooth muscle cell (SMC) depletion (Ramanath et al, 2009; Wang et al, 2012; An et al, 2017), elastic fiber fragmentation (Nakashima, 2010; Pratt and Curci, 2010; Roberts et al, 2011) and collagen degradation (Wang et al, 2006; Ren et al, 2014; Xu K. et al, 2018)
Angiotensin II (Ang II) promotes the infiltration of macrophages and the secretion of matrix metalloproteinases (MMPs) via the axis of Kruppel-like factor 6 and granulocyte macrophage-colonystimulating factor (GM-CSF) (Son et al, 2015), as well as a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS-1) (Gao et al, 2016), to cause local inflammation and Studies have shown that macrophages secrete a variety of factors associated with AD, including metalloproteinases, ILs, vascular endothelial growth factor (VEGF), and others
Summary
Reviewed by: Suowen Xu, University of Rochester, United States Sivareddy Kotla, The University of Texas MD Anderson Cancer Center, United States. 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. 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. 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
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