Aortic Aneurysms

Kuivaniemi, Helena; Platsoucas, Chris D.; Tilson, M. David

doi:10.1161/circulationaha.107.690982

Cited by 194 publications

(109 citation statements)

References 90 publications

(106 reference statements)

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“…Particularly reduced to one or two studies are the investigations on the role of immune/inflammatory SNPs in sporadic TAA. Nevertheless, it is in increasing the opinion of scientific community to consider this pathology an immune disease, as well as its evidence [25]. Based on this, we evaluated, for the first time, the role of TLR-4-mediated signaling pathway and ten related genetic variants in the risk of sporadic TAA and dissection [32,33].…”

Section: Discussionmentioning

confidence: 99%

“…Recent evidence proposes sporadic TAAD as an immune disease with a strong genetic component [25]. An active participation of both innate/inflammatory and clonotypic responses has been evidenced.…”

Section: Focus On the Role In Sporadic Taad Of Genetic Variants In Pamentioning

confidence: 99%

“…However, it is in increasing the opinion to consider the sporadic TAA forms as immune/inflammatory diseases with a strong genetic component [25]. As result, a better characterization at the molecular level of sporadic TAA is necessary.…”

Section: Introductionmentioning

confidence: 99%

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Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Balistreri

2015

Vascular Pharmacology

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Keywords:Sporadic thoracic aortic aneurysms (TAA) and dissections Genetic variants Biomarkers Targets for new personalized therapeutic treatments Sporadic thoracic aortic aneurysms (TAA) and dissections are one of the major causes of morbidity and mortality worldwide, especially in those older than 65 years. The presentation of TAA is varied and often silent. Thus, sporadic TAA detection is often fortuitous, with identification occurring during a routine physical examination or during an unrelated medical evaluation. Once suspected, confirmation by imaging clinical approaches is needed to allow the choose of the unique treatments for TAA, namely the surgery procedures, including elective surgery or endovascular repair before the onset of catastrophic and fatal complications, such as dissection or rupture. At present, there are no biomarkers available to identify TAAs before visible symptoms. However, recent progresses in understanding of molecular and cellular mechanisms involved in the patho-physiology of sporadic TAA are suggesting different molecular pathways and their genetic variants as potential biomarkers, which might be applied into TAA clinical practice in the near future. Here, we report literature evidence on some disease pathways and their genetic variants on TAA susceptibility and compliances, and their translation as promising TAA preventive and prognostic biomarkers and targets for new personalized therapeutic treatments.

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Section: Discussionmentioning

confidence: 99%

Section: Focus On the Role In Sporadic Taad Of Genetic Variants In Pamentioning

confidence: 99%

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Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Balistreri

2015

Vascular Pharmacology

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“…One of the defining characteristics of AAA is inflammation accompanied by a cellular infiltrate that is predominantly lymphocytic (6)(7)(8). The elastase-induced AAA mouse model recapitulates many key features of human AAA, including the inflammatory response (9).…”

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confidence: 99%

Fibrinogen-specific antibody induces abdominal aortic aneurysm in mice through complement lectin pathway activation

Zhou

Yan

Bertram

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Abdominal aortic aneurysm (AAA) is a common vascular disease associated with high mortality rate due to progressive enlargement and eventual rupture. There is currently no established therapy known to alter the rate of aneurysmal expansion. Thus, understanding the processes that initiate and sustain aneurysmal growth is pivotal for the development of medical therapies aimed at halting disease progression. Using an elastase-induced AAA mouse model that recapitulates key features of human AAA, we previously reported that a natural IgG antibody directs alternative pathway complement activation and initiates the inflammatory process that culminates in aneurysmal development. The target of this natural antibody, however, was unknown. Herein we identify a natural IgG that binds to fibrinogen deposited in elastaseperfused aortic tissues, activates the complement lectin pathway (LP), and induces AAA. Moreover, we establish that alterations in the glycosylation patterns of this antibody critically affect its ability to activate the LP in vivo. We find that LP activation precedes the alternative pathway and absence of the LP complement protein mannan-binding lectin abrogates elastase-induced AAA. In human AAA tissues the mouse anti-fibrinogen antibody recognizes epitopes that localize to the same areas that stain positively for mannan-binding lectin, which suggests that the complement LP is engaged in humans as well. Lastly, we demonstrate that circulating antibodies in a subset of AAA patients react against fibrinogen or fibrinogen-associated epitopes in human aneurysmal tissues. Our findings support the concept that an autoimmune process directed at aortic wall self-antigens may play a central role in the immunopathogenesis of AAA.A bdominal aortic aneurysm (AAA) is a common vascular disorder that affects ∼5% of men and ∼1.5% of women ages 65 and older (1, 2). Rupture of AAA presents a medical emergency that accounts for 15,000 deaths annually in the United States (3). Currently, surgical repair represents the only treatment option for large AAAs, whereas surgery in small AAAs offers no clear overall long-term survival advantage (4, 5). Thus, medical management, to inhibit or reverse the progression of small AAAs, has received increasing attention. Major challenges remain in the development of therapeutic agents that impede aneurysm expansion, as our understanding of the pathophysiology underlying this disease is incomplete.One of the defining characteristics of AAA is inflammation accompanied by a cellular infiltrate that is predominantly lymphocytic (6-8). The elastase-induced AAA mouse model recapitulates many key features of human AAA, including the inflammatory response (9). We previously established with this model that aneurysm development requires factor B and properdin of the complement alternative pathway (AP) (10, 11). We showed that mice deficient in B cells (and hence antibodies), called μMT mice, are protected against aneurysm formation. Reconstitution with natural IgG, but not IgM, from wild-type mice res...

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“…The cellular infiltrate of macrophages and lymphocytes represents the major cell types in human aneurysms and are located mainly in the tunica adventitia 5 . Besides promoting leukocyte infiltration and cytokine production, the adventitial layer is highly reactive and may play a significant role in the formation of aneurysms.…”

Section: Results Results Results Resultsmentioning

confidence: 99%

Efeitos da remoção da túnica adventícia da aorta descendente em suínos

Fagundes¹,

Pereira

Correa

et al. 2012

Rev. Col. Bras. Cir.

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OBJETIVO: Investigar os efeitos da remoção da adventícia da aorta em suínos. MÉTODOS: O experimento foi realizado com oito suínos. Removeu-se a camada adventícia da aorta descendente. Após a eutanásia com duas, quatro, seis e oito semanas, o segmento aórtico era removido. Após, eram feitos cortes histológicos com a coloração de hematoxilina e eosina (HE) e pelo método de Weigert - Van Gieson. RESULTADOS: Após duas semanas identificou-se um leve desarranjo do terço externo da túnica média. Nos animais sacrificados após quatro semanas observou-se um desarranjo estrutural dos terços externos da túnica média. Após seis semanas observou-se necrose da parede aórtica. Finalmente, após oito semanas além da fibrose da parede aórtica identificou-se a destruição da lâmina elástica interna. CONCLUSÃO: A remoção da adventícia da aorta em suínos levou à alterações degenerativas da média, determinando perda da estrutura da parede aórtica que é variável em sua localização, intensidade e forma, dependendo do tempo a partir do qual se estabeleceu a lesão isquêmica.

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Aortic Aneurysms

Cited by 194 publications

References 90 publications

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

Fibrinogen-specific antibody induces abdominal aortic aneurysm in mice through complement lectin pathway activation

Efeitos da remoção da túnica adventícia da aorta descendente em suínos

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