Interleukin-18 Expression Increases in the Aorta and Plasma of Patients with Acute Aortic Dissection

Hu, Haiying; Zhang, Guangtai; Hu, Huanli; Liu, Wenjing; Liu, Jixiang; Xin, Shuanli; Zhao, Xiufeng; Han, Liying; Duan, Liping; Huang, Xinshun; Chang, Chao

doi:10.1155/2019/8691294

Cited by 19 publications

(15 citation statements)

References 35 publications

(39 reference statements)

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“…Previous studies have shown that IL-6 signaling is mediated by macrophage activation in Ang IIinduced vascular disease (Schuett et al, 2009), and that the IL-6-STAT3 model pathway regulates the downstream Th7-IL-17 axis and upregulates monocyte macrophage activity (Ju et al, 2013). IL-18 may promote M1 macrophage differentiation and increase macrophage-induced apoptosis of SMCs (Hu et al, 2019). Taken together, it appears that macrophages secrete ILs to promote local inflammation of the aortic wall, while receiving regulatory signals from ILs to further expand the inflammatory response, for the ultimate promotion of AD.…”

Section: Effects Of Ils On the Aortic Wallmentioning

confidence: 99%

The Role of Macrophages in Aortic Dissection

et al. 2020

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Aortic dissection (AD) is a fatal disease that accounts for a large proportion of aorticrelated 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.

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Section: Effects Of Ils On the Aortic Wallmentioning

confidence: 99%

The Role of Macrophages in Aortic Dissection

et al. 2020

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“…14 Development of a mouse model that demonstrated unregulated TGF-b resulted from the altered matrix in fibrillin-1 deficiency, paved the way for research into the immunological basis of aortic diseases including AAS (Table 2). 10,11,14,[16][17][18][19][20][21][22][23][24][25] Immunohistochemical studies have examined the role of inflammation in AAS in detail, particularly for AD. One study tested patients' serum monocyte level and found it to be higher in those with AD.…”

Section: Immunological Basis Of Aasmentioning

confidence: 99%

“…Interleukin-18 18 Produced by immune cells such as T lymphocytes, macrophages, and vascular smooth muscle cells.…”

Section: Seen In a Mouse Model Of Aortic Dissectionmentioning

confidence: 99%

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Immunological therapeutics in acute aortic syndrome

Rimmer

Moughal

Bashir

2020

Asian Cardiovasc Thorac Ann

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Acute aortic syndrome is a group of interlinked conditions with common presenting symptoms, including aortic dissection, penetrating atherosclerotic ulcer, and intramural hematoma. Pharmacological management of acute aortic syndrome is a growing area, with key themes to address the underlying inflammatory pathways believed to be the cause. Research into interleukins, matrix metalloproteinases, and granulocyte macrophage colony-stimulating factor are just some of the many immunological properties being investigated and translated into medical therapies. Stem cell experiments may indicate further advances in the pathologies of acute aortic syndrome. The study of pharmacogenomics to improve treatment across different genomes is also a novel area outlined in this paper.

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“…3 The histopathology of aortic aneurysm and dissection involves loss of small muscle cells and elastin fibers resulting in medial degeneration, and aortic wall softening. 4,5 High aortic wall tension due to acute or chronic pressure load enhances aneurysm formation and the extent of dissection. 2 The severity of the aortic wall degeneration may be associated with the propagation of aortic dissection.…”

Section: Introductionmentioning

confidence: 99%

Increased Epicardial Adipose Tissue is Associated with the Extent of Aortic Dissection

Emlek

Yılmaz

Özer

et al. 2020

Journal of the Saudi Heart Association

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Background: Epicardial adipose tissue (EAT) is a biologically active organ that has endocrine and paracrine functions. Endothelial dysfunction, systemic, and local inflammatory response, due to bio-active molecules produced by EAT, may affect aortic dissection propagation and extent. We investigated the association between EAT thickness and the extent of aortic dissection. Methods: We retrospectively enrolled 78 patients with aortic dissection diagnosed by thoracoabdominal Computerized Tomography (CT). EAT was measured from the thickest part of the perpendicular plane between the pericardium and free wall of the right ventricle using CT. Aortic dissection length was measured from the beginning to the end of the dissection flap at sagittal images. Results: We included 78 patients with the mean age of 63.9 ± 11.7 and 57 (73.5%) patients were male. Dissection length was correlated positively with EAT (r ¼ 0.409, p < 0.001), body mass index (r ¼ 0.408, p ¼ 0.018), and admission systolic blood pressure (r ¼ 0.830, p ¼ 0.026) whereas an inverse correlation existed between age and dissection length (r ¼ ¡0.318, p ¼ 0.005). Multivariate analysis identified age and EAT as independent predictors of dissection length. Conclusion: Increased EAT was independently associated with the extent of aortic dissection. We think that either paracrine and endocrine functions of EAT might have contributed to the extent of aortic dissection.

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Interleukin-18 Expression Increases in the Aorta and Plasma of Patients with Acute Aortic Dissection

Cited by 19 publications

References 35 publications

The Role of Macrophages in Aortic Dissection

The Role of Macrophages in Aortic Dissection

Immunological therapeutics in acute aortic syndrome

Increased Epicardial Adipose Tissue is Associated with the Extent of Aortic Dissection

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