Lack of C4d deposition may reveal susceptibility for ascending aortic dissection

Niinimaki, Eetu; Paavonen, Timo; Valo, Timo; Tarkka, Matti; Mennander, Ari

doi:10.3109/14017431.2012.663502

Cited by 7 publications

(5 citation statements)

References 18 publications

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“…Inflammatory conditions of the aorta, including aortitis and vasculitis, may be associated with degeneration of the medial and adventitial layers of the aortic wall [43]. Both immunoglobulin G4 and complement 4d have been reported to be involved in the pathogenesis of aortic dissection [44,45], whereas giant-cell and Takayasu arteritis are associated with a T-cell-mediated inflammation of the vasa vasori, potentially leading to aneurysm formation and fibrotic stenosis of the aorta [46].…”

Section: Risk Factorsmentioning

confidence: 99%

Acute type A aortic dissection – a review

Guðbjartsson

Ahlsson

Geirsson

et al. 2019

Scandinavian Cardiovascular Journal

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Acute type A aortic dissection (ATAAD) is still one of the most challenging diseases that cardiac surgeons encounter. This review is based on the current literature and includes the results from the Nordic Consortium for Acute Type-A Aortic Dissection (NORCAAD) database. It covers different aspects of ATAAD and concentrates on the outcome of surgical repair. The diagnosis is occasionally delayed, and ATAAD is usually lethal if prompt repair is not performed. The dynamic nature of the disease, the variation in presentation and clinical course, and the urgency of treatment require significant attentiveness. Many surgical techniques and perfusion strategies of varying complexity have been described, ranging from simple interposition graft to total arch replacement with frozen elephant trunk and valve-sparing root reconstruction. Although more complex techniques may provide long-term benefit in selected patients, they require significant surgical expertise and experience. Short-term survival is first priority so an expedited operation that fits in with the surgeon's level of expertise is in most cases appropriate. ARTICLE HISTORY Definitions and classification systemsDissection of the aorta occurs when the aortic media is separated, usually by pulsatile flow that penetrates the intimal layer of the aortic wall [14] (Figure 1(b)). This allows blood to flow between the layers of the aortic wall, forcing the layers apart, creating a false lumen parallel to the native (i.e. true) aortic lumen (Figure 1(b)). Consequently, the false lumen can propagate in both directions from the tear of intima and affect most of its distal branches, including the coronary, cerebral, and mesenteric arteries [15]. Another-but less common-CONTACT Tomas Gudbjartsson

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Section: Risk Factorsmentioning

confidence: 99%

Acute type A aortic dissection – a review

Guðbjartsson

Ahlsson

Geirsson

et al. 2019

Scandinavian Cardiovascular Journal

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“…This may provide the evidence that the C3-inducing AAAs are not specific, and some proper anti-C3 drugs may work in attenuating the development of AAAs. Another complement component C4d, however, shows a protective role in some inflammatory aortic disease such as aortic dissection [ 65 ].…”

Section: Innate Immunitymentioning

confidence: 99%

Modulation of Immune-Inflammatory Responses in Abdominal Aortic Aneurysm: Emerging Molecular Targets

Bai

et al. 2018

Journal of Immunology Research

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Abdominal aortic aneurysm (AAA), a deadly vascular disease in human, is a chronic degenerative process of the abdominal aorta. In this process, inflammatory responses and immune system work efficiently by inflammatory cell attraction, proinflammatory factor secretion and subsequently MMP upregulation. Previous studies have demonstrated various inflammatory cell types in AAA of human and animals. The majority of cells, such as macrophages, CD4+ T cells, and B cells, play an important role in the diseased aortic wall through phenotypic modulation. Furthermore, immunoglobulins also greatly affect the functions and differentiation of immune cells in AAA. Recent evidence suggests that innate immune system, especially Toll-like receptors, chemokine receptors, and complements are involved in the progression of AAAs. We discussed the innate immune system, inflammatory cells, immunoglobulins, immune-mediated mechanisms, and key cytokines in the pathogenesis of AAA and particularly emphasis on a further trend and application of these interventions. This current understanding may offer new insights into the role of inflammation and immune response in AAA.

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“…Although all three pathways of complement are known to be involved in the development of AAA, less is known regarding the potential role of complement in aortic dissection. A previous study suggested that C4d deposition (complement activation) is a predictive marker for susceptibility to ascending aortic dissection (38).…”

Section: Discussionmentioning

confidence: 99%

The Complement C3a–C3aR Axis Promotes Development of Thoracic Aortic Dissection via Regulation of MMP2 Expression

Ren

Liu

Wang

et al. 2018

The Journal of Immunology

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Thoracic aortic dissection (TAD), once ruptured, is devastating to patients, and no effective pharmaceutical therapy is available. Anaphylatoxins released by complement activation are involved in a variety of diseases. However, the role of the complement system in TAD is unknown. We found that plasma levels of C3a, C4a, and C5a were significantly increased in patients with TAD. Elevated circulating C3a levels were also detected in the developmental process of mouse TAD, which was induced by β-aminopropionitrile monofumarate (BAPN) treatment, with enhanced expression of C1q and properdin in mouse dissected aortas. These findings indicated activation of classical and alternative complement pathways. Further, expression of C3aR was obviously increased in smooth muscle cells of human and mouse dissected aortas, and knockout of C3aR notably inhibited BAPN-induced formation and rupture of TAD in mice. C3aR antagonist administered pre- and post-BAPN treatment attenuated the development of TAD. We found that C3aR knockout decreased matrix metalloproteinase 2 (MMP2) expression in BAPN-treated mice. Additionally, recombinant C3a stimulation enhanced MMP2 expression and activation in smooth muscle cells that were subjected to mechanical stretch. Finally, we generated MMP2-knockdown mice by in vivo MMP2 short hairpin RNA delivery using recombinant adeno-associated virus and found that MMP2 deficiency significantly reduced the formation of TAD. Therefore, our study suggests that the C3aC3aR axis contributes to the development of TAD via regulation of MMP2 expression. Targeting the C3a-C3aR axis may represent a strategy for inhibiting the formation of TAD.

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Lack of C4d deposition may reveal susceptibility for ascending aortic dissection

Abstract: Lack of C4d may indicate active remodeling of the aortic wall leading to aortic dissection (AD). Immunologic complement factors may be amenable to diagnosis of instability after aortic surgery.

Cited by 7 publications

References 18 publications

Acute type A aortic dissection – a review

Acute type A aortic dissection – a review

Modulation of Immune-Inflammatory Responses in Abdominal Aortic Aneurysm: Emerging Molecular Targets

The Complement C3a–C3aR Axis Promotes Development of Thoracic Aortic Dissection via Regulation of MMP2 Expression

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